Publications by authors named "Daqing Zhao"

116 Publications

Ginsenosides repair UVB-induced skin barrier damage in BALB/c hairless mice and HaCaT keratinocytes.

J Ginseng Res 2022 Jan 10;46(1):115-125. Epub 2021 May 10.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin, China.

Background: Ginsenosides (GS) have potential value as cosmetic additives for prevention of skin photoaging. However, their protective mechanisms against skin barrier damage and their active monomeric constituents are unknown.

Methods: GS monomer types and their relative proportions were identified. A UVB-irradiated BALB/c hairless mouse model was used to assess protective effects of GS components on skin epidermal thickness and transepidermal water loss (TEWL). Skin barrier function, reflected by filaggrin (FLG), involucrin (IVL), claudin-1 (Cldn-1), and aquaporin 3 (AQP3) levels and MAPK phosphorylation patterns, were analyzed in UVB-irradiated hairless mice or HaCaT cells.

Results: Total GS monomeric content detected by UPLC was 85.45% and was largely attributed to 17 main monomers that included Re (16.73%), Rd (13.36%), and Rg1 (13.38%). In hairless mice, GS ameliorated UVB-induced epidermal barrier dysfunction manifesting as increased epidermal thickness, increased TEWL, and decreased stratum corneum water content without weight change. Furthermore, GS treatment of UVB-irradiated mice restored protein expression levels and epidermal tissue distributions of FLG, IVL, Cldn-1, and AQP3, with consistent mRNA and protein expression results obtained in UVB-irradiated HaCaT cells (except for unchanging Cldn-1 expression). Mechanistically, GS inhibited JNK, p38, and ERK phosphorylation in UVB-irradiated HaCaT cells, with a mixture of Rg2, Rg3, Rk3, F2, Rd, and Rb3 providing the same protective MAPK pathway inhibition-associated upregulation of IVL and AQP3 expression as provided by intact GS treatment.

Conclusion: GS protection against UVB-irradiated skin barrier damage depends on activities of six ginsenoside monomeric constituents that inhibit the MAPK signaling pathway.
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http://dx.doi.org/10.1016/j.jgr.2021.05.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8753432PMC
January 2022

Ginseng in vascular dysfunction: A review of therapeutic potentials and molecular mechanisms.

Phytother Res 2022 Jan 13. Epub 2022 Jan 13.

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.

Vascular dysfunction can lead to a variety of fatal diseases, including cardiovascular and cerebrovascular diseases, metabolic syndrome, and cancer. Although a large number of studies have reported the therapeutic effects of natural compounds on vascular-related diseases, ginseng is still the focus of research. Ginseng and its active substances have bioactive effects against different diseases with vascular dysfunction. In this review, we summarized the key molecular mechanisms and signaling pathways of ginseng, its different active ingredients or formula in the prevention and treatment of vascular-related diseases, including cardiac-cerebral vascular diseases, hypertension, diabetes complications, and cancer. Moreover, the bidirectional roles of ginseng in promoting or inhibiting angiogenesis have been highlighted. We systematically teased out the relationship between ginseng and vascular dysfunction, which could provide a basis for the clinical application of ginseng in the future.
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http://dx.doi.org/10.1002/ptr.7369DOI Listing
January 2022

Compound traditional Chinese medicine dermatitis ointment ameliorates inflammatory responses and dysregulation of itch-related molecules in atopic dermatitis.

Chin Med 2022 Jan 4;17(1). Epub 2022 Jan 4.

Changchun University of Chinese Medicine, Changchun, Jilin, China.

Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease accompanied with itchy and scaly rash. Compound traditional Chinese medicine dermatitis ointment (CTCMDO) consists of a mixture of extracts from five plants, which had been used in AD treatment due to good anti-inflammatory and anti-allergic effects.

Materials And Methods: In this study, high-performance liquid chromatography (HPLC) and liquid chromatography/mass spectrometer (LC/MS) were performed to analyze the active ingredients of CTCMDO in detail and to establish its HPLC fingerprint. Furthermore, the anti-inflammatory and antipruritic activities of CTCMDO were studied in the treatment of DNCB-induced AD in mice.

Results: A total of 44 compounds including phenylpropionic acid compounds, alkaloid compounds, curcumin compounds and lignans were identified via combined HPLC and LC/MS. A fingerprint with 17 common peaks was established. In AD-like mice, DNCB-induced scratching behavior had been suppressed in the treatment of CTCMDO in a dose-dependent manner. Furthermore, the detailed experimental results indicated that the AD can be effectively improved via inhibiting the production of Th1/2 cytokines in serum, reversing the upregulation of substance P levels of itch-related genes in the skin, and suppressing the phosphorylation of JNK, ERK, and p38 in the skin.

Conclusion: This work indicated that CTCMDO can significantly improve AD via attenuating the pathological alterations of Th1/2 cytokines and itch-related mediators, as well as inhibiting the phosphorylation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB).
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http://dx.doi.org/10.1186/s13020-021-00555-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8725352PMC
January 2022

Network Pharmacology and Experimental Assessment to Explore the Pharmacological Mechanism of Qimai Feiluoping Decoction Against Pulmonary Fibrosis.

Front Pharmacol 2021 3;12:770197. Epub 2021 Dec 3.

Institute of Metabolic Diseases, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

Pulmonary fibrosis (PF) is one of the pathologic changes in COVID-19 patients in convalescence, and it is also a potential long-term sequela in severe COVID-19 patients. Qimai Feiluoping decoction (QM) is a traditional Chinese medicine formula recommended in the Chinese national medical program for COVID-19 convalescent patients, and PF is one of its indications. Through clinical observation, QM was found to improve the clinical symptoms and pulmonary function and reduce the degree of PF of COVID-19 convalescent patients. To further explore the pharmacological mechanisms and possible active components of QM in anti-PF effect, UHPLC/Q-TOF-MS was used to analyze the composition of the QM extract and the active components that can be absorbed into the blood, leading to the identification of 56 chemical compounds and 10 active components. Then, network pharmacology was used to predict the potential mechanisms and targets of QM; it predicted that QM exerts its anti-PF effects the regulation of the epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) degradation, and TGF-β signaling pathway. Finally, TGF-β1-induced A549 cells were used to verify and explore the pharmacological effects of QM and found that QM could inhibit the proliferation of TGF-β1-induced A549 cells, attenuate EMT, and promote ECM degradation by inhibiting the TGF-β/Smad3 pathway.
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http://dx.doi.org/10.3389/fphar.2021.770197DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8678473PMC
December 2021

A Protein from (Chinese Yam) Improves Hydrocortisone-Induced Testicular Dysfunction by Alleviating Leydig Cell Injury via Upregulation of the Nrf2 Pathway.

Oxid Med Cell Longev 2021 30;2021:3575016. Epub 2021 Nov 30.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, 1035 Boshuo Road, Changchun, Jilin Province, China.

Leydig cell injury has been described as a primary driver of testicular dysfunction and is affected by oxidative stress. (Chinese yam) is used to improve testicular dysfunction in clinical and pharmacological research via its antioxidative activity, but the mechanisms underlying the beneficial effect of Chinese yam on testicular dysfunction and its suppression of Leydig cell oxidative damage remain unclear. In this study, we obtained a Chinese yam protein (DP1) and explored its effectiveness and possible mechanism in improving testicular dysfunction in vivo and in vitro. We established a testicular dysfunction model in rats using hydrocortisone (HCT). DP1 increased body weight and organ index, improved the deterioration in testicular morphology (including increasing the diameter of seminiferous tubules and thickness of germinal cell layers, inhibiting testicular cell apoptosis by increasing the Bcl-2/Bax ratio, and impeding collagen leakage by downregulating TGF-1 and p-SMAD2/3 expression), and restored the testosterone content. In addition, DP1 enhanced the number of Leydig cells in rats and HO-induced TM3 Leydig cells, and the effect of DP1 on the apoptosis, fibrosis, and testosterone content of TM3 cells was similar to that observed in vivo. These changes were dependent on the regulation of oxidative stress, including significantly reduced intracellular 8-hydroxy-2-deoxyguanosine levels, enhanced superoxide dismutase activities, and decreased superoxide anion levels, which were confirmed via a superoxide overexpression system. Furthermore, we observed that DP1 promoted Nrf2 nuclear import and upregulated antioxidant factor expression in vivo and in vitro. However, Nrf2 silencing eliminated the ability of DP1 to increase the Bcl-2/Bax ratio, reduce the expression levels of TGF-1 and p-SMAD2/3, and increase testosterone contents in HO-induced TM3 cells. In conclusion, DP1 reversed the HCT-induced testicular apoptosis and fibrosis and decreased testosterone contents by alleviating Leydig cell oxidative damage via upregulation of the Nrf2 pathway.
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http://dx.doi.org/10.1155/2021/3575016DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8651383PMC
November 2021

20(S)-Ginsenoside Rh2-induced apoptosis and protective autophagy in cervical cancer cells by inhibiting AMPK/mTOR pathway.

Biosci Biotechnol Biochem 2021 Dec;86(1):92-103

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin, China.

20(S)-Ginsenoside Rh2 (GRh2) has various biological activities including anticancer effects. However, no reports have investigated the connection between autophagy and apoptosis in HeLa cells treated with 20(S)-GRh2. In this study, we found that 20(S)-GRh2 suppressed proliferation and induced apoptosis in HeLa cells by activating the intrinsic apoptotic pathway and causing mitochondrial dysfunction. 20(S)-GRh2 enhanced cell autophagy through promoting the phosphorylation of AMPK, depressed the phosphorylation of AKT, and suppressed mTOR activity. Furthermore, treatment with the autophagy inhibitor 3-methyladenine (3-MA) enhanced 20(S)-GRh2-induced apoptosis, while the autophagy inducer rapamycin promoted cell survival. Moreover, the apoptosis inhibitor Z-VAD-FMK significantly restrained the apoptosis and autophagy induced by 20(S)-GRh2 in HeLa cells. We found that 20(S)-ginsenoside Rh2-induced protective autophagy promotes apoptosis of cervical cancer cells by inhibiting AMPK/mTOR pathway.
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http://dx.doi.org/10.1093/bbb/zbab189DOI Listing
December 2021

Nfib promotes chondrocyte proliferation and inhibits differentiation by mildly regulating Sox9 and its downstream genes.

Mol Biol Rep 2021 Nov 15;48(11):7487-7497. Epub 2021 Oct 15.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, China.

Background: Chondrocyte proliferation and differentiation play pivotal roles in regulating cartilage formation, endochondral bone formation, and repair. Cartilage damage and underdevelopment may cause severe joint diseases. Various transcription factors regulate cartilage development. Nuclear factor 1 B (Nfib) is a transcription factor that plays a regulatory role in various organs. However, the effect and mechanism of Nfib on the proliferation and differentiation of chondrocytes in cartilage are still largely unknown.

Methods And Results: In the present study, we investigated the gene expression patterns in primary chondrocytes with Nfib overexpression or silencing by RNA sequencing (RNA-seq) technology. The results showed that Nfib overexpression significantly up-regulated genes that are related to chondrocyte proliferation and extracellular matrix (ECM) synthesis and significantly down-regulated genes related to chondrocyte differentiation and ECM degradation. However, with Nfib silencing, the genes involved in promoting chondrocyte differentiation were significantly up-regulated, whereas those involved in promoting chondrocyte proliferation were significantly down-regulated. Furthermore, quantitative real-time PCR (qRT-PCR), western blot, alcian blue staining and immunofluorescence staining assays further confirmed that Nfib potentially promotes chondrocyte proliferation and extracellular synthesis but inhibits differentiation.

Conclusions: The molecular mechanism of Nfib in promoting chondrocyte proliferation and inhibiting differentiation was probably achieved by stimulating Sox9 and its downstream genes. Thus, this study adds new insights regarding the underlying molecular mechanism of transcriptional regulation in cartilage.
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http://dx.doi.org/10.1007/s11033-021-06767-2DOI Listing
November 2021

Ginseng root extract attenuates inflammation by inhibiting the MAPK/NF-κB signaling pathway and activating autophagy and p62-Nrf2-Keap1 signaling in vitro and in vivo.

J Ethnopharmacol 2022 Jan 11;283:114739. Epub 2021 Oct 11.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin, 130117, China. Electronic address:

Ethnopharmacological Relevance: Panax ginseng C.A. Meyer is a type of herbal plant that has frequently been used in many Asian countries to treat a variety of diseases. Ginseng is considered to exhibit anti-inflammatory and anti-oxidative pharmacological effects. However, the specific mechanism is still not entirely understood.

Aim Of The Study: In this study, we investigated if ginseng extract could attenuate inflammation and oxidative stress in RAW264.7 cells and in dextran sulfate sodium (DSS)-induced colitis mouse model.

Materials And Methods: RAW264.7 cells and LPS were used to develop inflammatory and oxidative cell models. C57/6J male mice and DSS were used to construct the animal models. O2-, mitochondria number, and mitochondrial membrane potential were analyzed using fluorescent probes and fluorescence microscopy. Reactive oxygen species and nitric oxide generation were detected with probes and microplate readers. The secreted amounts of inflammatory cytokines were measured by enzyme-linked immunosorbent assay kits. Protein expression levels in the cytoplasm and nucleus were measured by western blotting analyses. Quantitative real-time PCR (qRT-PCR) was used to determine the changes in mRNA levels. Autophagosome accumulation was analyzed by transmission electron microscopy. A p62-specific siRNA was used to evaluate the effect of p62 on the anti-oxidative function of ginseng root extract (GRE). Asperuloside and SP600125 were used to confirm the involvement of the MAPK/NF-κB signaling pathway.

Results: We performed a systematic analysis of the anti-inflammatory, anti-oxidative, and autophagy regulatory mechanisms of GRE in LPS-treated RAW264.7 cells. GRE considerably reduced the levels of nitric oxide, TNF-α, and IL-6 secreted by LPS-treated cells. GRE treatments dose-dependently upregulated IL-10 mRNA levels and decreased IL-6 and IL-1β mRNA levels in LPS-treated cells. Similar to the NF-κB and JNK inhibitors, GRE treatment significantly inhibited NF-κB activity and phosphorylation of MAPKs (JNK, ERK-1/2, and p38). Additionally, GRE treatment remarkably decreased LPS-triggered reactive oxygen species production and mitochondrial dysfunction by motivating Nrf2 nuclear translocation by enhancing phosphorylated p62. Knockdown of p62 resulted in the loss of GRE anti-oxidative ability. Autophagy was strongly induced by GRE via the Akt-mTOR signaling pathway, relieving excessive oxidation, mitochondrial dysfunction, and inflammation, while enhancing Beclin-1, LC3 II, and Atg7 protein expression. Furthermore, GRE alleviated the degree of injury, inflammatory cytokine production, and regulated the relative signaling pathway in DSS-induced colitis.

Conclusions: GRE can exert both anti-inflammatory and anti-oxidative functions by targeting the MAPK/NF-κB and p62-Nrf2-Keap1 pathways, as well as autophagy, in vitro and vivo.
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http://dx.doi.org/10.1016/j.jep.2021.114739DOI Listing
January 2022

Comprehensive RNA sequencing in primary murine keratinocytes and fibroblasts identifies novel biomarkers and provides potential therapeutic targets for skin-related diseases.

Cell Mol Biol Lett 2021 Oct 3;26(1):42. Epub 2021 Oct 3.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, China.

Background: Keratinocytes and fibroblasts represent the major cell types in the epidermis and dermis of the skin and play a significant role in maintenance of skin homeostasis. However, the biological characteristics of keratinocytes and fibroblasts remain to be elucidated. The purpose of this study was to compare the gene expression pattern between keratinocytes and fibroblasts and to explore novel biomarker genes so as to provide potential therapeutic targets for skin-related diseases such as burns, wounds, and aging.

Methods: Skin keratinocytes and fibroblasts were isolated from newborn mice. To fully understand the heterogeneity of gene expression between keratinocytes and fibroblasts, differentially expressed genes (DEGs) between the two cell types were detected by RNA-seq technology. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the known genes of keratinocytes and fibroblasts and verify the RNA-seq results.

Results: Transcriptomic data showed a total of 4309 DEGs (fold-change > 1.5 and q-value < 0.05). Among them, 2197 genes were highly expressed in fibroblasts and included 10 genes encoding collagen, 16 genes encoding transcription factors, and 14 genes encoding growth factors. Simultaneously, 2112 genes were highly expressed in keratinocytes and included 7 genes encoding collagen, 14 genes encoding transcription factors, and 8 genes encoding growth factors. Furthermore, we summarized 279 genes specifically expressed in keratinocytes and 33 genes specifically expressed in fibroblasts, which may represent distinct molecular signatures of each cell type. Additionally, we observed some novel specific biomarkers for fibroblasts such as Plac8 (placenta-specific 8), Agtr2 (angiotensin II receptor, type 2), Serping1 (serpin peptidase inhibitor, clade G, member 1), Ly6c1 (lymphocyte antigen 6 complex, locus C1), Dpt (dermatopontin), and some novel specific biomarkers for keratinocytes such as Ly6a (lymphocyte antigen 6 complex, locus A) and Lce3c (late cornified envelope 3C), Ccer2 (coiled-coil glutamate-rich protein 2), Col18a1 (collagen, type XVIII, alpha 1) and Col17a1 (collagen type XVII, alpha 1). In summary, these data provided novel identifying biomarkers for two cell types, which can provide a resource of DEGs for further investigations.
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http://dx.doi.org/10.1186/s11658-021-00285-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8489068PMC
October 2021

Screening and Comparison of Anti-Intestinal Inflammatory Activities of Three Polysaccharides from the Mycelium of Lion's Mane Culinary-Medicinal Mushroom, Hericium erinaceus (Agaricomycetes).

Int J Med Mushrooms 2021 ;23(9):63-71

Research Center of Traditional Chinese Medicine, Affiliated Hospital, Changchun University of Chinese Medicine, Changchun, 130021, China; Jilin Provincial Key Laboratory of BioMacromolecules of Chinese Medicine, Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130021, China.

Three major polysaccharides (wHEP-1, wHEP-2, and wHEP-3) were isolated from the mycelium of Hericium erinaceus. This study assessed their chemical and physical properties, molecular weight, monosaccharide compositions, and anti-ulcerative colitis ability to protect Caco-2 cells from lipopolysaccharide (LPS)-induced inflammation. The results showed that the average molecular weight of wHEP-1, wHEP-2, and wHEP-3 was 5010, 1812, and 1118 Da, respectively. wHEP-1 was composed of mannose, glucose, and galactose in a molar ratio of 1.2:16.9:1:1, whereas wHEP-2 and wHEP-3 were composed of glucose and galactose in different molar ratios. Anti-inflammatory activity was compared using LPS-induced Caco-2 cells and a rat model. wHEP-1 exhibited the best anti-inflammatory activity. Thus, the polysaccharide from H. erinaceus as a natural material shows potential for the development of alternative therapies.
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http://dx.doi.org/10.1615/IntJMedMushrooms.2021039951DOI Listing
November 2021

Protective effect of oligosaccharides isolated from Panax ginseng C. A. Meyer against UVB-induced skin barrier damage in BALB/c hairless mice and human keratinocytes.

J Ethnopharmacol 2022 Jan 23;283:114677. Epub 2021 Sep 23.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin Province, China; Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Changchun University of Chinese Medicine, Changchun, Jilin Province, China. Electronic address:

Ethnopharmacological Relevance: Skin barrier dysfunction can lead to water and electrolyte loss, triggering homeostatic imbalances that can trigger atopic dermatitis and anaphylaxis. Panax ginseng C.A. Meyer is a traditional Chinese medicinal herb with known therapeutic benefits for the treatment of skin diseases, including photodamage repair effects and reduction of pigmentation. However, few reports exist that describe effectiveness of ginseng active components for repair of skin barrier damage.

Materials And Methods: Ginseng oligosaccharide extract (GSO) was prepared from P. ginseng via water extraction followed by ethanol precipitation and resin and gel purification. GSO composition and structural characteristics were determined using LC-MS, HPLC, FT-IR, and NMR. To evaluate GSO as a skin barrier repair-promoting treatment, skin of UVB-irradiated BALB/c hairless mice was treated with or without GSO then skin samples were evaluated for epidermal thickness, transepidermal water loss (TEWL), and stratum corneum water content. In addition, UVB-exposed skin samples and HaCaT cells were analyzed to assess GSO treatment effects on levels of epidermal cornified envelope (CE) protein and other skin barrier proteins, such as filaggrin (FLG), involucrin (IVL), and aquaporin-3 (AQP3). Meanwhile, GSO treatment was also evaluated for effects on UVB-irradiated hairless mouse skin and HaCaT cells based on levels of serine protease inhibitor Kazal type-5 (SPINK5), trypsin-like kallikrein-related peptidase 5 (KLK5), chymotrypsin-like KLK7, and desmoglein 1 (DSG1). These proteins are associated with UVB-induced skin barrier damage manifesting as dryness and desquamation.

Results: GSO was shown to consist of oligosaccharides comprised of seven distinct types of monosaccharides with molecular weights of approximately 1 kDa that were covalently linked together via β-glycosidic bonds. In vivo, GSO applied to dorsal skin of BALB/c hairless mice attenuated UVB-induced epidermal thickening and moisture loss. Furthermore, GSO ameliorated UVB-induced reductions of levels of FLG, IVL, and AQP3 proteins. Additionally, GSO treatment led to increased DSG1 protein levels due to decreased expression of KLK7. In vitro, GSO treatment of UVB-irradiated HaCaT cells led to increases of FLG, IVL, and AQP3 mRNA levels and corresponding proteins, while mRNA levels of desquamation-related proteins SPINK5, KLK5, KLK7, and DSG1 and associated protein levels were restored to normal levels.

Conclusion: A P. ginseng oligosaccharide preparation repaired UVB-induced skin barrier damage by alleviating skin dryness and desquamation symptoms, highlighting its potential as a natural cosmetic additive that can promote skin barrier repair after UVB exposure.
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http://dx.doi.org/10.1016/j.jep.2021.114677DOI Listing
January 2022

Therapeutic Effects and Molecular Mechanisms of Bioactive Compounds Against Respiratory Diseases: Traditional Chinese Medicine Theory and High-Frequency Use.

Front Pharmacol 2021 27;12:734450. Epub 2021 Aug 27.

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.

Respiratory diseases, especially the pandemic of respiratory infectious diseases and refractory chronic lung diseases, remain a key clinical issue and research hot spot due to their high prevalence rates and poor prognosis. In this review, we aimed to summarize the recent advances in the therapeutic effects and molecular mechanisms of key common bioactive compounds from Chinese herbal medicine. Based on the theories of traditional Chinese medicine related to lung diseases, we searched several electronic databases to determine the high-frequency Chinese medicines in clinical application. The active compounds and metabolites from the selected medicines were identified using the Traditional Chinese Medicine Systems Pharmacology Database (TCMSP) by analyzing oral bioavailability and drug similarity index. Then, the pharmacological effects and molecular mechanisms of the selected bioactive compounds in the viral and bacterial infections, inflammation, acute lung injury (ALI), chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, asthma, and lung cancer were summarized. We found that 31 bioactive compounds from the selected 10 common Chinese herbs, such as epigallocatechin-3-gallate (EGCG), kaempferol, isorhamnetin, quercetin, and β-sitosterol, can mainly regulate NF-κB, Nrf2/HO-1, NLRP3, TGF-β/Smad, MAPK, and PI3K/Akt/mTOR pathways to inhibit infection, inflammation, extracellular matrix deposition, and tumor growth in a series of lung-related diseases. This review provides novel perspectives on the preclinical study and clinical application of Chinese herbal medicines and their bioactive compounds against respiratory diseases.
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http://dx.doi.org/10.3389/fphar.2021.734450DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8429615PMC
August 2021

Salicylic acid in ginseng root alleviates skin hyperpigmentation disorders by inhibiting melanogenesis and melanosome transport.

Eur J Pharmacol 2021 Nov 1;910:174458. Epub 2021 Sep 1.

Research Center of Traditional Chinese Medicine, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, 130021, China. Electronic address:

Abnormal melanogenesis and melanosome transport can cause skin pigmentation disorders that are often treated using ginseng-based formulation. We previously found that phenolic acid compounds in ginseng root could inhibit melanin production and as a skin-whitening agents. However, mechanisms of action underlying effects of ginseng phenolic acid monomers on melanogenesis remain unclear. This study was conducted to investigate effects of salicylic acid, a main ginseng root phenolic acid component, on melanogenesis and melanosome functions in melanocytes of zebrafish and other species. Salicylic acid exhibited no cytotoxicity and reduced melanin levels and tyrosinase activity in B16F10 murine melanoma cells and normal human epidermal melanocytes regardless of prior cell stimulation with α-melanocyte stimulating hormone. Additionally, salicylic acid treatment reduced expression of melanogenic enzymes tyrosinase, tyrosinase-related protein 1 and tyrosinase-related protein 2, while reducing expression of their master transcriptional regulator, microphthalmia-associated transcription factor. Moreover, reduced phosphorylation of cAMP response-element binding protein was observed due to reduced cAMP levels resulting from salicylic acid inhibition of upstream signal regulators (adenylyl cyclase and protein kinase A). Furthermore, salicylic acid treatment suppressed expression of transport complex-associated proteins melanophilin and myosin Va in two UVB-treated melanocytic cell lines, suppressed phagocytosis of fluorescent microspheres by UVB-stimulated human keratinocytes (HaCaT), inhibited protease-activated receptor 2 activation by reducing both Ca release and activation of phosphoinositide 3 kinase/AKT and mitogen-activated protein kinases and induced anti-melanogenic effects in zebrafish. Collectively, these results indicate that salicylic acid within ginseng root can inhibit melanocyte melanogenesis and melanin transport, while also suppressing keratinocyte phagocytic function.
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http://dx.doi.org/10.1016/j.ejphar.2021.174458DOI Listing
November 2021

Akt activation-dependent protective effect of wild ginseng adventitious root protein against UVA-induced NIH-3T3 cell damage.

Wound Repair Regen 2021 Nov 27;29(6):1006-1016. Epub 2021 Aug 27.

Research Centre of Traditional Chinese Medicine, First Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China.

Prolonged skin exposure to ultraviolet radiation can lead to development of several acute and chronic diseases, with UVA exposure considered a primary cause of dermal photodamage. We prepared a wild ginseng adventitious root extract (ARE) that could alleviate UVA irradiation-induced NIH-3T3 cell viability decline. After employing a series of purification methods to isolate main active components of ARE, adventitious root protein mixture (ARP) was identified then tested for protective effects against UVA irradiation-induced NIH-3T3 cell damage. The results showed that ARP treatment significantly reduced UVA-induced cell viability decline and confirmed that the active constituent of ARP was the protein, since proteolytic hydrolysis and heat treatment each eliminated ARP protective activity. Moreover, ARP treatment markedly inhibited UVA-induced apoptosis, cell cycle arrest and DNA fragmentation, while also significantly reversing UVA effects (elevated Bax levels, reduced Bcl-2 expression) by reducing Bax levels and increasing Bcl-2 expression. Mechanistically, ARP promoted Akt phosphorylation regardless of UVA exposure, thus confirming ARP resistance to inactivation by UVA light. Notably, in the presence of Akt inhibitor SC0227, ARP could no longer counteract UVA-induced cell viability decline and DNA fragmentation. Additionally, our results demonstrated that ARP treatment protected UVA-irradiated NIH-3T3 cells by preventing UVA-induced reduction of collagen-I expression. Taken together, these results suggest that ARP treatment of NIH-3T3 cells effectively mitigated UVA-induced cell viability decline by activating intracellular Akt to reduce UVA-induced DNA damage, leading to reduced rates of apoptosis and cell cycle arrest after UVA exposure and restoring collagen expression to normal levels.
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http://dx.doi.org/10.1111/wrr.12962DOI Listing
November 2021

Comparisons of Isolation Methods, Structural Features, and Bioactivities of the Polysaccharides from Three Common Panax Species: A Review of Recent Progress.

Molecules 2021 Aug 18;26(16). Epub 2021 Aug 18.

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun 130117, China.

spp. ( family) are widely used medicinal plants and they mainly include C.A. Meyer L. (American ginseng) and (notoginseng). Polysaccharides are the main active ingredients in these plants and have demonstrated diverse pharmacological functions, but comparisons of isolation methods, structural features, and bioactivities of these polysaccharides have not yet been reported. This review summarizes recent advances associated with 112 polysaccharides from ginseng, 25 polysaccharides from American ginseng, and 36 polysaccharides from notoginseng and it compares the differences in extraction, purification, structural features, and bioactivities. Most studies focus on ginseng polysaccharides and comparisons are typically made with the polysaccharides from American ginseng and notoginseng. For the extraction, purification, and structural analysis, the processes are similar for the polysaccharides from the three Panax species. Previous studies determined that 55 polysaccharides from ginseng, 18 polysaccharides from American ginseng, and 9 polysaccharides from notoginseng exhibited anti-tumor activity, immunoregulatory effects, anti-oxidant activity, and other pharmacological functions, which are mediated by multiple signaling pathways, including mitogen-activated protein kinase, nuclear factor kappa B, or redox balance pathways. This review can provide new insights into the similarities and differences among the polysaccharides from the three Panax species, which can facilitate and guide further studies to explore the medicinal properties of the family used in traditional Chinese medicine.
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http://dx.doi.org/10.3390/molecules26164997DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8400370PMC
August 2021

Comparison of Gene Expression Patterns in Articular Cartilage and Xiphoid Cartilage.

Biochem Genet 2021 Aug 19. Epub 2021 Aug 19.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, China.

Cartilage is a resilient and smooth connective tissue that is found throughout the body. Among the three major types of cartilage, namely hyaline cartilage, elastic cartilage, and fibrocartilage, hyaline cartilage is the most widespread type of cartilage predominantly located in the joint surfaces (articular cartilage, AC). It remains a huge challenge for orthopedic surgeons to deal with AC damage since it has limited capacity for self-repair. Xiphoid cartilage (XC) is a vestigial cartilage located in the distal end of the sternum. XC-derived chondrocytes exhibit strong chondrogenic differentiation capacity. Thus, XC could become a potential donor site of chondrocytes for cartilage repair and regeneration. However, the underlying gene expression patterns between AC and XC are still largely unknown. In the present study, we used state-of-the-art RNA-seq technology combined with validation method to investigate the gene expression patterns between AC and XC, and identified a series of differentially expressed genes (DEGs) involved in chondrocyte commitment and differentiation including growth factors, transcription factors, and extracellular matrices. We demonstrated that the majority of significantly up-regulated DEGs (XC vs. AC) in XC were involved in regulating cartilage regeneration and repair, whereas the majority of significantly up-regulated DEGs (XC vs. AC) in AC were involved in regulating chondrocyte differentiation and maturation. This study has increased our knowledge of transcriptional networks in hyaline cartilage and elastic cartilage. It also supports the use of XC-derived chondrocytes as a potential cell resource for cartilage regeneration and repair.
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http://dx.doi.org/10.1007/s10528-021-10127-xDOI Listing
August 2021

C. A. Meyer Phenolic Acid Extract Alleviates Ultraviolet B-Irradiation-Induced Photoaging in a Hairless Mouse Skin Photodamage Model.

Evid Based Complement Alternat Med 2021 2;2021:9962007. Epub 2021 Aug 2.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, China.

Here, we evaluated the skin-protective effects of topical applications of C. A. Meyer extract (PG2) and its phenolic acid- (PA-) based components against UVB-induced skin photoaging. PG2 or PA applied to skin of hairless mice after UVB-irradiation alleviated UVB-induced effects observed in untreated skin, such as increased transepidermal water loss (TEWL), increased epidermal thickness, and decreased stratum corneum water content without affecting body weight. Moreover, PG2 and PA treatments countered reduced mRNA-level expression of genes encoding filaggrin (FLG), transglutaminase-1 (TGM1), and hyaluronan synthases (HAS1, HAS2, and HAS3) caused by UVB exposure and reduced UVB-induced collagen fiber degradation by inhibiting the expression of matrix metalloproteinase genes encoding MMP-1, MMP-2, and MMP-9. Meanwhile, topical treatments reduced cyclooxygenase-2 (COX-2) mRNA-level expression in photodamaged skin, leading to the inhibition of interleukin-1 (IL-1) and interleukin-6 (IL-6) mRNA-level expression. Thus, ginseng phenolic acid-based preparations have potential value as topical treatments to protect skin against UVB-induced photoaging.
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http://dx.doi.org/10.1155/2021/9962007DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8356000PMC
August 2021

Identification of Jmjd3 as an Essential Epigenetic Regulator of Gene Temporal Collinear Activation for Body Axial Patterning in Mice.

Front Cell Dev Biol 2021 21;9:642931. Epub 2021 Jul 21.

Department of Otolaryngology, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.

Body axial patterning develops a rostral-to-caudal sequence and relies on the temporal colinear activation of genes. However, the underlying mechanism of gene temporal colinear activation remains largely elusive. Here, with small-molecule inhibitors and conditional gene knockout mice, we identified Jmjd3, a subunit of TrxG, as an essential regulator of temporal colinear activation of genes with its H3K27me3 demethylase activity. We demonstrated that Jmjd3 not only initiates but also maintains the temporal collinear expression of genes. However, we detected no antagonistic roles between Jmjd3 and Ezh2, a core subunit of PcG repressive complex 2, during the processes of axial skeletal patterning. Our findings provide new insights into the regulation of gene temporal collinear activation for body axial patterning in mice.
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http://dx.doi.org/10.3389/fcell.2021.642931DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8333871PMC
July 2021

Insight Into Polysaccharides From C. A. Meyer in Improving Intestinal Inflammation: Modulating Intestinal Microbiota and Autophagy.

Front Immunol 2021 20;12:683911. Epub 2021 Jul 20.

College of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.

Polysaccharides from C. A. Meyer (P. ginseng) are the main active component of P. ginseng and exhibit significant intestinal anti-inflammatory activity. However, the therapeutic mechanism of the ginseng polysaccharide is unclear, and this hinders the application for medicine or functional food. In this study, a polysaccharide was isolated from P. ginseng (GP). The primary structure and morphology of the GP were studied by HPLC, FT-IR spectroscopy, and scanning electron microscopy (SEM). Further, its intestinal anti-inflammatory activity and its mechanism of function were evaluated in experimental systems using DSS-induced rats, fecal microbiota transplantation (FMT), and LPS-stimulated HT-29 cells. Results showed that GP modulated the structure of gut microbiota and restored mTOR-dependent autophagic dysfunction. Consequently, active autophagy suppressed inflammation through the inhibition of NF-κB, oxidative stress, and the release of cytokines. Therefore, our research provides a rationale for future investigations into the relationship between microbiota and autophagy and revealed the therapeutic potential of GP for inflammatory bowel disease.
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http://dx.doi.org/10.3389/fimmu.2021.683911DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8329555PMC
October 2021

[Corrigendum] 20(s)‑ginseonside‑Rg3 modulation of AMPK/FoxO3 signaling to attenuate mitochondrial dysfunction in a dexamethasone‑injured C2C12 myotube‑based model of skeletal atrophy .

Mol Med Rep 2021 Sep 19;24(3). Epub 2021 Jul 19.

Research Center of Traditional Chinese Medicine, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin 130021, P.R. China.

Following the publication of this paper, the authors requested that Daqing Zhao also be included as a joint author for correspondence. The Editor has granted this request, and therefore, the revised information for the corresponding authors is presented as follows (changes highlighted in bold): MANYING WANG, RUI JIANG, JIANZENG LIU, XIAOHAO XU, GUANG SUN, DAQING ZHAO and LIWEI SUWN. Research Center of Traditional Chinese Medicine, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin 130021; Jilin Ginseng Academy, Changchun University of Chinese Medicine; Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Changchun, Jilin 130117, P.R. China. Correspondence to: Professor Liwei Sun, Research Center of Traditional Chinese Medicine, The Affiliated Hospital to Changchun University of Chinese Medicine, 1478 Gongnong Street, Changchun, Jilin 130021, P.R. China. E‑mail: [email protected] All the authors agree to this Corrigendum, and they are grateful to the Editor for allowing this Corrigendum to be published. [the original article was published in 23: Article no. 306, 2021; DOI: 10.3892/mmr.2021.11945].
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http://dx.doi.org/10.3892/mmr.2021.12259DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8261618PMC
September 2021

A Novel Biochemical Study of Anti-Dermal Fibroblast Replicative Senescence Potential of Oligosaccharides.

Front Pharmacol 2021 30;12:690538. Epub 2021 Jun 30.

Research Center of Traditional Chinese Medicine, the Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, China.

Dermal fibroblast replicative senescence that often occurs in aging skin is characterized by loss of cell proliferative capacity, cell cycle arrest, decreased cell elongation, and decreased synthesis of dermal extracellular matrix (ECM) components. Although is known for its effectiveness in alleviating many age-related degenerative diseases, few studies have evaluated components for efficacy or mechanisms of action in delaying cell replicative senescence. In this study, oligosaccharides (PNO) were isolated using a stepwise purification procedure involving water extraction and alcohol precipitation followed by DEAE Sepharose Fast Flow column chromatography, preparative high performance liquid chromatography, and size-exclusion chromatography. Monosaccharides detected in PNO constituents included mannose, galactose, and sorbitose in relative molar proportions of 14.2:12.3:1, respectively, aligning with PNO absorption spectrum results resembling typical known spectra for sugars. , PNO treatment of replicative senescent NIH-3T3 fibroblasts significantly promoted cell vitality, inhibited SA-β-galactosidase (SA-β-Gal) activity, and reduced p16 and p21 protein-level expression. Moreover, PNO treatment of senescent fibroblasts led to a lower proportion of G1 phase cells and higher proportion of S phase cells, while also inducing aging NIH-3T3 cells to migrate and synthesize collagen-I (CoL-I). Mechanistically, PNO treatment up-regulated expression of proliferating cell nuclear antigen (PCNA), cyclin E, cyclin D1, and cyclin-dependent kinase 4 (CDK4) proteins and promoted phosphorylation of MEK, p38, and ERK1/2 to trigger cell cycle progression. Additionally, PNO treatment also up-regulated protein-level expression of TGF-β1 and levels of p-Smad2/3, p-FAK, and p-Pax to trigger CoL-I synthesis and cell migration. Taken together, these findings demonstrate that oligosaccharides purified from could reverse fibroblast replicative senescence by promoting fibroblast cell proliferation, migration, and CoL-I production.
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http://dx.doi.org/10.3389/fphar.2021.690538DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8277921PMC
June 2021

Neuroprotective Potentials of Panax Ginseng Against Alzheimer's Disease: A Review of Preclinical and Clinical Evidences.

Front Pharmacol 2021 2;12:688490. Epub 2021 Jun 2.

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.

Alzheimer's disease (AD), a neurodegenerative disorder, is a major health concern in the increasingly aged population worldwide. Currently, no clinically effective drug can halt the progression of AD. C.A. Mey is a well-known medicinal plant that contains ginsenosides, gintonin, and other components and has neuroprotective effects against a series of pathological cascades in AD, including beta-amyloid formation, neuroinflammation, oxidative stress, and mitochondrial dysfunction. In this review, we summarize the effects and mechanisms of these major components and formulas containing in neuronal cells and animal models. Moreover, clinical findings regarding the prevention and treatment of AD with or its formulas are discussed. This review can provide new insights into the possible use of ginseng in the prevention and treatment of AD.
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http://dx.doi.org/10.3389/fphar.2021.688490DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8206566PMC
June 2021

Antiviral strategies targeting herpesviruses.

J Virus Erad 2021 Sep 30;7(3):100047. Epub 2021 May 30.

Changchun University of Chinese Medicine, Changchun, China.

Herpesviruses, known as large DNA viruses, have a wide host range. In addition to human beings, cattle, and horses, even carp can be hosts for herpesvirus infection. Herpesviruses are pathogens possessing elaborate mechanisms that regulate host cell components for its replication, assembly and generating mature virus particles that can infect humans and most animals, usually causing multiple and lifelong infections. In addition, several human diseases, such as genital or mouth herpes, mononucleosis, and Burkitt lymphoma, are usually associated with herpesvirus infection. Blocking the steps of viral infection, such as entry, replication and assembly, may be an effective way for many different herpes viruses and their related diseases. Therefore, we aim to describe antiviral agents that are able to prevent herpesvirus entry, replication and assembly in host cells. We summarize antiviral strategies, including certain small molecular drugs, RNA interference and CRISPR/Cas9 system-based antiviral approaches, which represent promising approaches.
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http://dx.doi.org/10.1016/j.jve.2021.100047DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187247PMC
September 2021

Ginsenoside extract from ginseng extends lifespan and health span in .

Food Funct 2021 Aug;12(15):6793-6808

Research Center of Traditional Chinese Medicine, the First Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, China.

Nutrition intervention has become a potential strategy to improve healthspan and prolong lifespan. Ginseng has been used for thousands of years and developed as a functional food to provide various protective effects to humans. An extract of total ginsenosides (TGS), a mixture of the main active ginsenosides from ginseng, has wide biological activities and health benefits for age-related diseases, including antioxidation and improvements in mitochondrial function. However, the molecular mechanism of TGS for prolonging lifespan and improving fitness and how exactly this is achieved under normal and stress conditions remain largely unclear. In this study, wild-type and mutant C. elegans strains are used to investigate the role and molecular mechanism of TGS-mediated longevity, health benefits, and stress resistance. The results showed that treatment with TGS at 0.2 mg mL-1 from the stage of day four to death significantly extended the lifespan of worms by 14.02% without effects on bacterial metabolism and food intake. Furthermore, TGS treatment obviously improved age-associated mobility, muscle fiber organization, lipofuscin accumulation, and enhanced resistance under oxidative stress. Importantly, these effects of TGS were achieved by activating the signaling pathways of anti-oxidant regulation and longevity, including the NRF2/SKN-1, SIRT1/SIR 2.1, and FOXO/DAF-16 signaling pathways. Finally, it was found that Rg1, Re, and Rb1 were the major effective components of anti-oxidative activity and longevity. Collectively, the protective effect of ginsenoside extract in healthy aging and stress responses provides new insights for the development and practical application of ginseng functional products.
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http://dx.doi.org/10.1039/d1fo00576fDOI Listing
August 2021

Review of ginsenosides targeting mitochondrial function to treat multiple disorders: Current status and perspectives.

J Ginseng Res 2021 May 11;45(3):371-379. Epub 2020 Dec 11.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin, China.

Mitochondrial dysfunction contributes to the pathogenesis and prognosis of many common disorders, including neurodegeneration, stroke, myocardial infarction, tumor, and metabolic diseases. Ginsenosides, the major bioactive constituents of , have been reported to play beneficial roles in the molecular pathophysiology of these diseases by targeting mitochondrial dysfunction. In this review, we first introduce the types of ginsenosides and basic mitochondrial functions. Then, recent findings are summarized on different ginsenosides targeting mitochondria and their key signaling pathways for the treatment of multiple diseases, including neurological disorders, cancer, heart disease, hyperglycemia, and inflammation are summarized. This review may explain the common targets of ginsenosides against multiple diseases and provide new insights into the underlying mechanisms, facilitating research on the clinical application of .
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http://dx.doi.org/10.1016/j.jgr.2020.12.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8134842PMC
May 2021

Total ginsenosides induce autophagic cell death in cervical cancer cells accompanied by downregulation of bone marrow stromal antigen-2.

Exp Ther Med 2021 Jul 22;22(1):667. Epub 2021 Apr 22.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, P.R. China.

Ginsenosides are important active components in . In the present study, total ginsenosides (TGNs) were demonstrated to enhance autophagy by promoting acidic vacuole organelle formation, recruitment of enhanced green fluorescent protein-microtubule-associated protein light chain 3 and expression of autophagy-related factors in cervical cancer cell lines. TGN markedly increased the expression of p62 at the transcriptional level, but decreased p62 protein expression in the presence of actinomycin D. The autophagic regulatory effect was reversible. TGN (≤120 µg/ml) did not affect the proliferation of cervical cancer cells under normal culture conditions, but markedly inhibited the growth of serum-deprived cells. Treatment with an inhibitor of autophagy (3-methyladenine) impaired TGN-induced cell death. This suggested that TGN caused autophagic cell death. In addition, western blot analysis demonstrated that the protein level of bone marrow stromal antigen-2 (BST-2) was downregulated by TGN. Upregulation of BST-2 reduced cell death. The results of the combined actions of various monomeric ginsenosides in TGN provide the molecular basis to develop TGN as a promising candidate for cancer therapy.
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http://dx.doi.org/10.3892/etm.2021.10099DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8112150PMC
July 2021

Knockdown of p62/sequestosome enhances ginsenoside Rh2-induced apoptosis in cervical cancer HeLa cells with no effect on autophagy.

Biosci Biotechnol Biochem 2021 Apr;85(5):1097-1103

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, Jilin, China.

p62/sequestosome is a multifunctional adaptor protein that participates in a wide variety of cellular processes. 20(S)-Ginsenoside Rh2 (G-Rh2) has various biological effects, including anticancer activity. We found that G-Rh2 can induce apoptosis and autophagy in HeLa cells. G-Rh2 significantly enhanced the transcriptional level of p62. A siRNA was constructed to knock down p62 and assess its effect on apoptosis induced by G-Rh2. p62 protein levels were successfully downregulated in cells transfected with the p62-specific siRNA. Silencing of p62 further decreased cell viability while also enhancing cell apoptosis, reactive oxygen species generation, the ratio of Bax to Bcl-2, and the cleavage of PARP. p62 knockdown decreased expression levels of Nrf2. Moreover, silencing of p62 had no significant effect on autophagy induced by G-Rh2. These results suggest that combining G-Rh2 treatment with inhibition of p62 may be a potential treatment strategy for cervical cancer.
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http://dx.doi.org/10.1093/bbb/zbab019DOI Listing
April 2021

20(s)‑ginseonside‑Rg3 modulation of AMPK/FoxO3 signaling to attenuate mitochondrial dysfunction in a dexamethasone‑injured C2C12 myotube‑based model of skeletal atrophy .

Mol Med Rep 2021 05 2;23(5). Epub 2021 Mar 2.

Research Center of Traditional Chinese Medicine, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin 130021, P.R. China.

Muscle atrophy, a side effect from administration of the anti‑inflammatory medication dexamethasone (DEX), is preventable by concomitant administration of the major monomeric constituent of C.A. Meyer, 20(S)‑ginsenoside Rg3 (S‑Rg3). Putative S‑Rg3‑associated prevention of DEX‑induced muscle atrophy may involve S‑Rg3 mitigation of DEX‑induced mitochondrial dysfunction. In the present study, MTT assays revealed enhanced cell viability following S‑Rg3 treatment of DEX‑injured C2C12 myotubes. Subsequent PCR and western blotting results demonstrated S‑Rg3‑induced reduction of expression of muscle atrophy F‑box protein (atrogin‑1) and muscle RING‑finger protein‑1, proteins previously linked to muscle atrophy. Additionally, S‑Rg3 treatment of DEX‑injured myotubes led to aggregation of Rg3 monomers in cells and dose‑dependent increases in cellular mitochondrial basal respiratory oxygen consumption rate and intracellular ATP levels compared with their levels in untreated DEX‑injured myotubes. In addition, S‑Rg3 treatment significantly reversed DEX‑induced reductions of expression of key mitochondrial respiratory electron transport chain subunits of protein complexes II, III and V in DEX‑injured myotube cells. Furthermore, S‑Rg3 alleviation of mitochondrial dysfunction associated with DEX‑induced injury of C2C12 myotubes was linked to S‑Rg3‑associated decreases in both forkhead box O3 (FoxO3) protein expression and phosphorylation of AMP‑activated protein kinase (AMPK). Collectively, these results implicate S‑Rg3 modulation of signaling within the AMPK‑FoxO3 pathway as a putative mechanism underlying S‑Rg3 alleviation of DEX‑induced muscle atrophy.
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http://dx.doi.org/10.3892/mmr.2021.11945DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7974265PMC
May 2021

Antioxidant, Anti-Inflammatory, and Cytotoxic Properties and Chemical Compositions of (Pall.) Maxim.

Evid Based Complement Alternat Med 2021 15;2021:6659620. Epub 2021 Feb 15.

Changchun University of Chinese Medicine, Changchun 130117, China.

(Pall.) Maxim. remains unexplored and underutilized resources with a high potential to improve human health. In this study, a new ursane-type triterpenoid, namely, 2, 3-dihydroxyurs-12-en-28-aldehyde (compound 10), and other 23 known compounds were isolated. 5 triterpenoids (compounds 6, 8, and 10-12), 11 flavonoids (compounds 13-15 and 17-24), 6 phenolic compounds (compounds 1, 2, 4, 5, 9, and 16), 2 sterols (compounds 3 and 7) were isolated from the aqueous solution extract of the aerial parts of . The structures of all compounds were elucidated by the use of extensive spectroscopic methods such as infrared spectroscopy (IR), high-resolution electrospray ionization mass spectrometry (HR-ESI-MS), H-NMR, and C-NMR. The solvent extractions of ethyl acetate fraction were evaluated for antioxidant activities using DPPH (2, 2-diphenyl-1-picrylhydrazyl) and ABTS (2, 2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid)) methods. The anti-inflammatory effects of the compounds were evaluated in lipopolysaccharide- (LPS-) stimulated RAW 264.7 macrophages. The extract cytotoxicity on the cancer cell lines MCF-7, HeLa, 4T1, and A549 was determined by MTT assay. As a result, compounds 10, 11, and 12 exhibited better antioxidant activity compared to the other compounds. Compounds 8-24 had different inhibitory effects on the release of NO, TNF-, and IL-6 in LPS-stimulated RAW 264.7 cells. The new compound has shown a significant inhibiting effect on cancer cells, and the cell inhibition rate increased in a dose-dependent manner. Further research to elucidate the chemical compositions and pharmacological effects of is of major importance towards the development and foundation of clinical application of the species.
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http://dx.doi.org/10.1155/2021/6659620DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7902150PMC
February 2021

The enzymatic hydrolysates from deer sinew promote MC3T3-E1 cell proliferation and extracellular matrix synthesis by regulating multiple functional genes.

BMC Complement Med Ther 2021 Feb 10;21(1):59. Epub 2021 Feb 10.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, China.

Background: Deer Sinew serves as a medicinal food, and has been used for treating skeletal diseases, especially bone diseases in a long history. Thus, it could become an alternative option for the prevention and therapeutic remedy of bone-related diseases. In our previous study, we established an optimal extraction process of the enzymatic hydrolysates from Chinese Sika deer sinews (DSEH), and we demonstrated that DSEH significantly promoted the proliferation of MC3T3-E1 cells (an osteoblast-like cell line) with a certain dose-effect relationship. However, the precise molecular mechanism of deer sinew in regulating bone strength is still largely unknown. The aim of this study was to explore the underlying molecular mechanism of DSEH on MC3T3-E1 cells proliferation and extracellular matrix synthesis.

Methods: Preparation and quality control were performed as previously described. The effect of DSEH at different administrated concentrations on cell proliferation was measured using both CCK-8 and MTT assays, and the capacity of DSEH on extracellular matrix synthesis was detected by Alizarin red staining and quantification. The gene expression pattern change of MC3T3-E1 cells under the treatment of DSEH was investigated by RNA-seq analysis accompanied with validation methods.

Results: We demonstrated that DSEH promoted MC3T3-E1 cell proliferation and extracellular matrix synthesis by regulating multiple functional genes. DSEH significantly increased the expression levels of genes that promoted cell proliferation such as Gstp1, Timp1, Serpine1, Cyr61, Crlf1, Thbs1, Ctgf, P4ha2, Sod3 and Nqo1. However, DSEH significantly decreased the expression levels of genes that inhibited cell proliferation such as Mt1, Cdc20, Gas1, Nrp2, Cmtm3, Dlk2, Sema3a, Rbm25 and Hspb6. Furthermore, DSEH mildly increased the expression levels of osteoblast gene markers.

Conclusions: Our findings suggest that DSEH facilitate MC3T3-E1 cell proliferation and extracellular matrix synthesis to consolidate bone formation and stability, but prevent MC3T3-E1 cells from oxidative stress-induced damage, apoptosis and further differentiation. These findings deepened the current understanding of DSEH on regulating bone development, and provided theoretical support for the discovery of optional prevention and treatment for bone-related diseases.
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http://dx.doi.org/10.1186/s12906-021-03240-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7877118PMC
February 2021
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