Publications by authors named "Jiyan Su"

27 Publications

  • Page 1 of 1

Vorinostat targets UBE2C to reverse epithelial-mesenchymal transition and control cervical cancer growth through the ubiquitination pathway.

Eur J Pharmacol 2021 Oct 29;908:174399. Epub 2021 Jul 29.

Foshan Maternal and Child Health Research Institute, South Medical University Affiliated Maternal & Child Health Hospital of Foshan, Foshan, 528000, China; School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China. Electronic address:

Vorinostat is a histone deacetylase inhibitor (HDACi) that was demonstrated in our previous study to inhibit the proliferation, migration, and invasion of cervical cancer cells by regulating the PI3K/Akt signaling pathway. However, the molecular mechanism of vorinostat in cervical cancer treatment remains to be further elucidated. A nude mouse xenograft model was established to analyze the antitumor effect of vorinostat in vivo. The combination of iTRAQ-based proteomics and parallel reaction monitoring (PRM) technology has proven to be an efficient and reliable method to identify potential targets for cancer chemotherapy. In this study, 254 differentially expressed proteins in vorinostat-treated cervical cancer cells, among which 180 were upregulated and 74 were downregulated, were identified by using an iTRAQ-based proteomic strategy. Subsequent bioinformatic and PRM analysis of these differentially expressed proteins indicated that UBE2C is a promising target of vorinostat in the inhibition of cervical cancer cell proliferation. We confirmed that the expression of endogenous UBE2C in cervical cancer cell lines was significantly higher than that in normal cervical epithelial cell lines. Additionally, we found that vorinostat downregulated the expression of UBE2C, SQSTM1/p62, N-cadherin, vimentin and upregulated E-cadherin in SiHa and HeLa cells. Our results also showed that vorinostat can downregulate the expression of SQSTM1/p62, N-cadherin, and vimentin during the treatment of cervical cancer cells by regulating UBE2C, while upregulating the expression of E-cadherin. In conclusion, vorinostat reverses epithelial-mesenchymal transition by targeting UBE2C and controls the proliferation of cervical cancer cells through the ubiquitination pathway. UBE2C can be used as a promising target for the development of vorinostat treatment strategies.
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http://dx.doi.org/10.1016/j.ejphar.2021.174399DOI Listing
October 2021

Polysaccharides of Sporoderm-Broken Spore of Modulate Adaptive Immune Function via Gut Microbiota Regulation.

Evid Based Complement Alternat Med 2021 23;2021:8842062. Epub 2021 Mar 23.

Department of Traditional Chinese Medicine, The People's Hospital of Dongying, Dongying, Shandong, China.

(Leyss.Fr.) Karst is one of the well-known medicinal macrofungi all over the world, and mounting researches have focused on the polysaccharides derived from the spores of . In the present study, BALB/c mice ( = 8-10) were administered with crude polysaccharides of spores (CPGS) and the refined polysaccharides of spores (RPGS) for 30 days to investigate their effect on the adaptive immune system. Results showed that CPGS and RPGS displayed diverse effects on the lymphocyte activity in the spleen. The splenocyte proliferation activity upon mitogen was suppressed by CPGS and RPGS, while the NK cell's tumor-killing ability was promoted by CPGS. Both CPGS and RPGS could increase the proportion of naïve T cells in thymus, but only RPGS significantly uplifted the percentage of T cells, as well as the T cell subsets, in peripheral blood, and promoted the activation by upregulating the expression of costimulatory factor CD28. Moreover, 16S sequencing results showed that the effects of CPGS and RPGS were closely related to the regulation of gut microbiota. -diversity of the microbiome was evidently changed by CPGS and RPGS. The phytoestrogen/polysaccharide-metabolizing bacteria (, , and ), and an unclassified , were remarkably enriched by CPGS or RPGS, and functions involving carbohydrate metabolism, membrane transport, and lipid metabolism were regulated. Moreover, the enrichments of , , and were positively related to the immune regulation by CPGS and RPGS, while that of displayed a negative correlation. These findings suggested a promising effect of the polysaccharide from sporoderm-broken spore of in immune regulation to promote health control.
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http://dx.doi.org/10.1155/2021/8842062DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8009716PMC
March 2021

Corrigendum to " Berry Polysaccharides Strengthen Gut Microenvironment and Modulate Gut Microbiota of the Mice".

Evid Based Complement Alternat Med 2020 25;2020:4840656. Epub 2020 Nov 25.

State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.

[This corrects the article DOI: 10.1155/2020/8097021.].
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http://dx.doi.org/10.1155/2020/4840656DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7710424PMC
November 2020

Ethanol extract of Centella asiatica alleviated dextran sulfate sodium-induced colitis: Restoration on mucosa barrier and gut microbiota homeostasis.

J Ethnopharmacol 2021 Mar 3;267:113445. Epub 2020 Oct 3.

Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, PR China; School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, PR China. Electronic address:

Ethnopharmacological Relevance: Ulcerative colitis (UC) is a relapsing inflammatory disease that still demands for effective remedies due to various adverse effects of the current principal treatments. Centella asiatica is a traditional medical herb with long application history in anti-inflammation.

Aim Of The Study: To explore the anti-inflammatory effect and possible mechanism of C. asiatica ethanol extract (CA) in a murine colitis model induced by dextran sulfate sodium (DSS).

Materials And Methods: CA was analyzed by high performance liquid chromatograph (HPLC). The colitis model was induced by free access to 3% DSS in distilled water for 7 days. CA (100, 200, and 400 mg/kg) and 5-aminosalicylic acid (5-ASA, 400 mg/kg) were administrated by gavage during the 7-day DSS challenge. At the end of experiment, mice were sacrificed and the brain, colon and cecum contents were harvested for analysis. Colitis was evaluated by disease activity index (DAI), colon length and colon lesion macroscopic score with hematoxylin-eosin staining. Myeloperoxidase (MPO) activity in colon and 5-hydroxytryptamine (5-HT) in brain were determined by ELISA. Tight junction protein expressions (ZO-1, E-Cadherin, Claudin-1) and c-Kit in colon were assessed by western blot and immunohistochemistry, respectively. Microbiota of cecum content was analyzed by 16S rRNA sequencing.

Results: Data showed that with recovery on the colon length and histological structure, CA prominently decreased DAI and macroscopic score for lesion in the suffering mice. CA relieved the colitis by suppressing inflammatory cell infiltration with decreased MPO activity in the colon, and up-regulated the expression of tight junction protein (ZO-1, E-cadherin) to enhance the permeability of intestinal mucosa. Moreover, CA restored intestinal motility by promoting c-Kit expression in the colon and 5-HT in the brain. Moreover, CA was able to reshape the gut microbiota in the suffering mice. It increased the α-diversity and shifted the community by depleting the colitis-associated genera, Helicobacter, Jeotgalicoccus and Staphylococcus, with impact on several metabolism signaling pathways, which possibly contributes to the renovation on the impaired intestinal mucosal barrier.

Conclusions: CA displayed the anti-inflammatory activity against the DSS-induced colitis, which would possibly rely on the restoration on mucosa barrier and gut microbiota homeostasis, highlights a promising application of C. asiatica in the clinical treatment of UC.
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http://dx.doi.org/10.1016/j.jep.2020.113445DOI Listing
March 2021

Polysaccharide from spore of Ganoderma lucidum ameliorates paclitaxel-induced intestinal barrier injury: Apoptosis inhibition by reversing microtubule polymerization.

Biomed Pharmacother 2020 Oct 5;130:110539. Epub 2020 Aug 5.

Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, PR China; Mathematical Engineering Academy of Chinese Medicine, Dongguan, Guangdong, PR China; National Egnieering Research Center for Modernazation of Traditional Chinese Medicine, Guangzhou, Guangdong, PR China. Electronic address:

Side effects of chemotherapy are burning questions for physicians and patients involved in cancers. Ganoderma lucidum is a widely consumed traditional Chinese medicine and edible mushroom with multiple functional properties. The present study aims to investigate the potential of polysaccharides from spore of G. lucidum (SGP) on small intestinal barrier function recovery against paclitaxel (PTX) challenge in a breast cancer mice model and IEC-6 cell line. The 4T1 tumor-bearing mice were treated with PTX together with four-week daily oral administration of SGP. Results indicated that combination of PTX and SGP reversed body weight lost and remolded the histology of small intestine, accompanied with promoted proliferation but suppressed apoptosis in intestinal cells. Intestinal barrier function was enhanced by the combination as indicated by reduced endotoxemia and the up-regulation of tight junction proteins, including Zonula occludens-1 (ZO-1), E-cadherin, β-catenin and Occludin. The protection of SGP was further confirmed in IEC-6 cells affected by PTX in vitro. The combination treatment prevented PTX-induced apoptosis in IEC-6 by inhibiting microtubule polymerization, and the aforementioned tight junction proteins were also upregulated. These findings suggest a promising protective effect of SGP against small intestinal barrier injury caused by PTX, highlighting its clinical implication against the chemotherapy side effects.
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http://dx.doi.org/10.1016/j.biopha.2020.110539DOI Listing
October 2020

Ethanol extract of Pycnoporus sanguineus relieves the dextran sulfate sodium-induced experimental colitis by suppressing helper T cell-mediated inflammation via apoptosis induction.

Biomed Pharmacother 2020 Jul 11;127:110212. Epub 2020 May 11.

Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, PR China. Electronic address:

Inflammatory bowel disease (IBD) is a chronic relapsing inflammation involving the gut system, and disequilibrium of T helper (Th) cell paradigm has been recognized as critical pathogenesis. Pycnoporus sanguineus (L.) Murrill is a species of the white-rot basidiomycetes listed as food- and cosmetic-grade microorganisms. In this study, anti-inflammatory activity of the ethanol extract from P. sanguineus (PSE) was investigated in dextran sulfate sodium (DSS)-induced experimental colitis model. PSE recovered the DSS-caused weight loss, reversed the colon shortening, and ameliorated the histopathological lesion in colon, resulting in lower disease activity index (DAI). Levels of serumal lipopolysaccharide (LPS), colonic myeloperoxidase (MPO) in the colitis-suffering mice were declined by PSE treatment. PSE also improved the mucosal integrity by enhancing the expression of tight junction and adherens junction proteins in the colon, including ZO-1, occludin, claudin-1, and E-cadherin. Besides, PSE reduced helper T cells (Th) in the colon, together with an evident decrease of several Th cell-related cytokines. Moreover, it was found that in vitro, PSE suppressed T cells and the Th subset upon Concanavalin A (ConA)-stimulation by inducing apoptosis. In summary, PSE displayed a remission on the colitis-related inflammation, which would possibly rely on the epithelial barrier restoration by suppressing Th cells via apoptosis induction, highlighting a promising potential in the treatment for IBD.
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http://dx.doi.org/10.1016/j.biopha.2020.110212DOI Listing
July 2020

Ethanol Extract of Seed Inhibit Triple-Negative Breast Cancer by Restraining Autophagy via PI3K/Akt/mTOR Pathway.

Front Pharmacol 2020 29;11:606. Epub 2020 Apr 29.

Department of Thyroid and Breast Surgery, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Triple-negative breast cancer (TNBC) is an aggressive disease with worst prognosis than other subtypes of breast cancer. Owing to the lack of hormone receptors and HER2 expression on TNBC cells, patients do not have targeted therapy options available with other breast cancer subtypes. Extensive efforts have been made to identify novel therapeutics against TNBC. Interestingly, recent studies had shown that plant-derived natural products could modulate the autophagy and induce the breast cancer cells death. Seed of has been used as an important traditional Chinese medicine against cancers. In the present study, the anti-breast cancer potential of ethanol crude extracts from seed (BJE) was explored. Data demonstrated that BJE could inhibit the TNBC cell line MDA-MB-231 proliferation and induced apoptosis. In the cells exposed to BJE, protein expressions of UNC-51-like kinase-1 (ULK1) and Beclin-1 and the ratio of light chain 3 II/I (LC3 II/I) were reduced, while the expression of p62 was increased, indicating an inhibition on autophagy. Moreover, BJE promoted the phosphorylation of mammalian target of rapamycin (mTOR), phosphatidylinositol 3-kinase (PI3K), and Akt in MDA-MB-231. BJE also suppressed the MDA-MB-231 tumor growth . Coincide with the results , autophagy in the tumor tissue was weakened as indicated by decreased ratio of LC 3 II/I and Beclin-1 accompanied by enhanced phosphorylation of mTOR, which confirmed that autophagy restraint via the PI3K/Akt/mTOR signaling pathway contributes to the suppression by BJE. Notably, no noticeable toxicity in non-targeted organs was found, including small intestine, liver, and kidney. Taken together, this study revealed anti-breast cancer activity of BJE based on autophagy restraint, highlighting its clinical importance as a novel natural agent against TNBC.
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http://dx.doi.org/10.3389/fphar.2020.00606DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7201043PMC
April 2020

Polysaccharide from Pycnoporus sanguineus ameliorates dextran sulfate sodium-induced colitis via helper T cells repertoire modulation and autophagy suppression.

Phytother Res 2020 Oct 13;34(10):2649-2664. Epub 2020 Apr 13.

Guangdong Laboratory Animals Monitoring Institute, Guangdong Provincial Key Laboratory of Laboratory Animals, Guangzhou, Guangdong, People's Republic of China.

Inflammatory bowel disease (IBD) is a chronic autoimmune disease associated with various risk factors. Pycnoporus sanguineus (L.) Murrill is a saprotrophic fungus used worldwide for its industrial and medical purposes. Here, polysaccharide from P. sanguineus (PPS) was explored for its antiinflammatory potential in a murine colitis model of IBD induced by dextran sulfate sodium (DSS). PPS ameliorated the colitis as manifested by the lowered disease activity index (DAI), prolonged colon, and reduced serum lipopolysaccharide (LPS). PPS recovered the histological lesion by upregulating the expressions of Zonula occludens-1 (ZO-1), E-cadherin, and proliferating cell nuclear antigen (PCNA). PPS inhibited the helper T cells (Th)-mediated immune response by decreasing the proportions of Th cells (including Th2 cells, Th17 cells, and regulatory T cells), which was accompanied with reductions on myeloperoxidase (MPO) activity and releases of several interleukins and chemokines within the colon. Moreover, PPS exhibited an evident inhibition on autophagy, in which the ratio of light chain 3 (LC3) II/I was declined, while the expression of p62 and Beclin-1 was increased. The present study highlighted important clinical implications for the treatment application of PPS against IBD, which relies on the regulation of Th cells repertoire and autophagy suppression to restore epithelium barrier.
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http://dx.doi.org/10.1002/ptr.6695DOI Listing
October 2020

Preparation, physicochemical characterization, and anti-proliferation of selenium nanoparticles stabilized by Polyporus umbellatus polysaccharide.

Int J Biol Macromol 2020 Jun 19;152:605-615. Epub 2020 Feb 19.

State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, Guangdong Open Laboratory of Applied Microbiology, Guangdong Institute of Microbiology, Guangdong Academy of Sciences, Guangzhou 510070, China; Guangdong Yuewei Edible Fungi Technology Co. Ltd., Guangzhou 510663, China. Electronic address:

Selenium nanoparticles (SeNPs), a novel selenium form, have attracted worldwide attention due to their bioactivities and low toxicity. This study aimed to assess the physicochemical characterization, storage stability, and anti-proliferative activities of SeNPs stabilized by Polyporus umbellatus polysaccharide (PUP). Results showed that orange-red, zero-valent, amorphous and spherical SeNPs with mean diameter of approximately 82.5 nm were successfully prepared by using PUP as a capping agent. PUP-SeNPs solution stored at 4 °C in dark condition could be stable for at least 84 days. Moreover, PUP-SeNPs treatment inhibited four cancer cell lines proliferation in a dose-dependent manner, while no significant cytotoxicity towards three normal cell lines was observed. Comparing with the other cancer cell lines (HepG2, Hela, and HT29), PUP-SeNPs displayed the most sensitive towards MDA-MB-231 cells with an IC value of 6.27 μM. Furthermore, PUP-SeNPs significantly up-regulated Bax/Bcl-2 ratio, promoted cytochrome c release, increased caspase-9, -8 and -3 activities, and poly (ADP-ribose) polymerase cleavage, suggesting that mitochondria-mediated and death receptor-mediated apoptotic pathways were activated in MDA-MB-231 cells. Besides, PUP-SeNPs possessed better anti-proliferative activity than selenomethionine as well as lower cytotoxicity than sodium selenite. Taken together, PUP-SeNPs have strong potential as a dietary supplement for application in cancer chemoprevention, especially breast cancer.
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http://dx.doi.org/10.1016/j.ijbiomac.2020.02.199DOI Listing
June 2020

Corrigendum: Anti-breast Cancer Enhancement of a Polysaccharide From Spore of With Paclitaxel: Suppression on Tumor Metabolism With Gut Microbiota Reshaping.

Front Microbiol 2019 31;10:1224. Epub 2019 May 31.

School of Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, China.

[This corrects the article DOI: 10.3389/fmicb.2018.03099.].
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http://dx.doi.org/10.3389/fmicb.2019.01224DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6555303PMC
May 2019

Anti-breast Cancer Enhancement of a Polysaccharide From Spore of With Paclitaxel: Suppression on Tumor Metabolism With Gut Microbiota Reshaping.

Front Microbiol 2018 17;9:3099. Epub 2018 Dec 17.

School of Pharmaceutical Science, Guangzhou University of Chinese Medicine, Guangzhou, China.

Increasing evidence highlights the cardinal role of gut microbiota in tumorigenesis and chemotherapy outcomes. Paclitaxel (PTX), although as a first-line chemotherapy reagent for breast cancer, still requires for improvement on its efficacy and safety due to drug resistance and adverse effects. The present work explored the enhancement of a polysaccharide derived from spore of (SGP) with PTX in a murine 4T1-breast cancer model. Results showed that the combination of PTX and SGP displayed an improved tumor control, in which mRNA expression of several Warburg effect-related proteins, i.e., glucose transporter 3 (), lactate dehydrogenase A (), and pyruvate dehydrogenase kinase (), and the metabolite profile of tumor was evidently altered. Flowcytometry analysis revealed that the combination treatment recovered the exhausted tumor infiltration lymphocytes (TILs) via inhibiting the expressions of immune checkpoints (PD-1 and Tim-3), while PTX alone evidently increased that of CTLA-4. 16S rRNA sequencing revealed a restoration by the combination treatment on gut microbiota dysbiosis induced by PTX, especially that , and other 5 genera were significantly enriched while the cancer-risk genera, and , were decreased. Moreover, spearman correlation analysis showed that abundance of was significantly negative-associated with the amount of frucotose-6-phosphate within the tumor. Collectively, the present study suggests the clinical implication of SGP as an adjuvant candidate for PTX against breast cancer, which possibly relies on the regulation of tumor metabolism and gut microbiota.
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http://dx.doi.org/10.3389/fmicb.2018.03099DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304348PMC
December 2018

Antitumor Activity of Extract From the Sporoderm-Breaking Spore of : Restoration on Exhausted Cytotoxic T Cell With Gut Microbiota Remodeling.

Front Immunol 2018 31;9:1765. Epub 2018 Jul 31.

State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, Guangdong Institute of Microbiology, Guangzhou, China.

As breast cancer is the leading cause of cancer-related deaths in women population worldwide, ongoing endeavor has been made for alternative regimens with improved efficacy but fewer adverse effects. Recently, active components from the spores of have attracted much attention for their versatile biological activities owing to the advance in sporoderm-breaking technology. Here, anticancer potential of an extract derived from the sporoderm-breaking spores of (ESG) was explored in a 4T1-breast cancer xenograft mice model. Results showed that ESG was able to suppress 4T1 tumor growth rather than . Flowcytometry analysis revealed that ESG could significantly increase both cytotoxic T cell (Tc) population and the ratio of Tc to helper T cell (Th) in peripheral blood of the tumor-bearing mouse; similar promotion on Tc was also found in tumor-infiltrating lymphocyte. Moreover, ESG evidently downregulated the two immune checkpoints, programmed cell death protein-1 (PD-1, in the spleen) and cytotoxic T lymphocyte antigen-4 (CTLA-4, in the tumor), suggesting that ESG could effectively restore the T cell paradigm by recovering the exhaustion status suppressing the co-inhibitory checkpoints. By 16S rRNA gene sequence analysis on the fecal microbiota, it was found that ESG would remodeling the overall structure of the samples from tumor-bearing mice toward that of the normal counterparts, including 18 genera in 5 phyla, together with regulations on several genes that are responsible for signaling pathways involved in metabolism, cellular processes, and environmental information processing. Collectively, this study demonstrated that ESG would serve as a natural anticancer adjuvant a restoration on the exhausted Tc, highlighting important clinical implications for the treatment of breast cancer.
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http://dx.doi.org/10.3389/fimmu.2018.01765DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6079217PMC
September 2019

Hypouricemic Effects of Extracts From on Hyperuricemia Mice and Virtual Prediction of Bioactives by Molecular Docking.

Front Pharmacol 2018 15;9:498. Epub 2018 May 15.

State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application and Guangdong Open Laboratory of Applied Microbiology, Guangdong Institute of Microbiology, Guangzhou, China.

has long been utilized for promoting diuresis in traditional Chinese medicine (TCM) with a close correlation to hypouricemia. Ethanol (AAE) and water (AAW) extracts of the compound led to a remarkable decrease in serum uric acid levels (SUA) in hyperuricemia mice, approaching that of the normal control. Both AAE and AAW exhibited suppression effects on hepatic xanthine oxidase (XOD) activities and elevation effects on renal OAT1 (organic anion transporter 1). However, only little negative impact was observed on the inner organ functions. The molecular docking was used to screen our in-home compound database for , and four compounds including 2-formyl-3,5-dihydroxybenzyl acetate, 2,4-dihydroxy-6-methylbenzaldehyde, 2-(6-hydroxy-1H-indol-3-yl)acetamide, and 6-hydroxy-1H-indole-3-carbaldehyde (HHC) were identified as potential active compounds. Their inhibitory mechanism on XOD might be attributed to their localization in the tunnel for the entrance of substrates to XOD active site, preventing the entrance of the substrates. To confirm the activity of the screened compounds experimentally, HHC was selected due to its high ranking and availability. The assaying result suggested the significant inhibitory activity of HHC on XOD. Also, these compounds were predicted to carry good ADME (absorption, distribution, metabolism, and excretion) properties, thereby necessitating further investigation. The current results provided an insight into the hypouricemic effects of macrofungi and their bioactives, which might provide the significant theoretical foundation for identifying and designing novel hypouricemia compounds.
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http://dx.doi.org/10.3389/fphar.2018.00498DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5962791PMC
May 2018

Hypouricemic Effects of Armillaria mellea on Hyperuricemic Mice Regulated through OAT1 and CNT2.

Am J Chin Med 2018 29;46(3):585-599. Epub 2018 Mar 29.

* State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application and Guangdong Open Laboratory of Applied Microbiology, Guangdong Institute of Microbiology, Guangzhou 510070, P. R. China.

Ethanol and water extracts of Armillaria mellea were prepared by directly soaking A. mellea in ethanol (AME) at 65[Formula: see text]C, followed by decocting the remains in water (AMW) at 85[Formula: see text]C. Significantly, AME and AMW at 30, 60 and 120[Formula: see text]mg/kg exhibited excellent hypouricemic actions, causing remarkable declines from hyperuricemic control (351[Formula: see text][Formula: see text]mol/L, [Formula: see text]) to 136, 130 and 115[Formula: see text][Formula: see text]mol/L and 250, 188 and 152[Formula: see text][Formula: see text]mol/L in serum uric acid, correspondingly. In contrast to the evident renal toxicity of allopurinol, these preparations showed little impacts. Moreover, they showed some inhibitory effect on XOD (xanthine oxidase) activity. Compared with hyperuricemic control, protein expressions of OAT1 (organic anion transporter 1) were significantly elevated in AME- and AMW-treated mice. The levels of GLUT9 (glucose transporter 9) expression were significantly decreased by AMW. CNT2 (concentrative nucleoside transporter 2), a key target for purine absorption in gastrointestinal tract was involved in this study, and was verified for its innovative role. Both AME and AMW down-regulated CNT2 proteins in the gastrointestinal tract in hyperuricemic mice. As they exhibited considerable inhibitory effects on XOD, we selected XOD as the target for virtual screening by using molecular docking, and four compounds were hit with high ranks. From the analysis, we concluded that hydrogen bond, Pi-Pi and Pi-sigma interactions might play important roles for their orientations and locations in XOD inhibition.
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http://dx.doi.org/10.1142/S0192415X18500301DOI Listing
July 2018

Cordycepin, a Characteristic Bioactive Constituent in , Ameliorates Hyperuricemia through URAT1 in Hyperuricemic Mice.

Front Microbiol 2018 25;9:58. Epub 2018 Jan 25.

Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.

Recently, we've reported the anti-hyperuricemic effects of . As a characteristic compound of , we hypothesized that cordycepin may play a role in preventing hyperurecimia. Remarkably, cordycepin produced important anti-hyperuricemic actions, decreasing SUA (serum uric acid) to 216, 210, and 203 μmol/L ( < 0.01) at 15, 30, and 60 mg/kg in comparison of hyperuricemic control (337 μmol/L), closing to normal control (202 μmol/L). Elisa, RT-PCR and western blot analysis demonstrated that the actions may be attributed to its downregulation of uric acid transporter 1 (URAT1) in kidney. Serum creatinine levels and blood urine nitrogen and liver, kidney, and spleen coefficients demonstrated that cordycepin may not impact liver, renal, and spleen functions. In addition, we used computational molecular simulation to investigate the binding mechanism of cordycepin. Of which, van der Waals interaction dominated the binding. Residues TRP290, ARG17, ALA408, GLY411, and MET147 contributed mainly on nonpolar energy. This provided the theoretical guidance to rationally design and synthesis novel URAT1 inhibitors.
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http://dx.doi.org/10.3389/fmicb.2018.00058DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5788910PMC
January 2018

Hypouricemic Effects of in Hyperuricemia Mice through OAT1 and GLUT9.

Front Pharmacol 2017 15;8:996. Epub 2018 Jan 15.

Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.

() dispels wind to eliminate dampness and exhibited nephron- and liver-protective effects as noted in Chinese herbal classic literature; it might also affect hyperuricemia. Therefore, we examined the hypouricemia effects and mechanisms underlying on chemical-induced hyperuricemia in mice. Ethanol (GAE) and water (GAW) extracts were prepared by extracting in ethanol (GAE), followed by bathing the remains in water to yield GAW. GAE and GAW were administered orally at different doses to hyperuricemia mice, while allopurinol and benzbromarone served as positive controls. Both GAE and GAW showed remarkable hypouricemia activities, rendering a substantial decline in the SUA (serum uric acid) level in hyperuricemia control ( < 0.01). Moreover, the urine uric acid (UUA) levels were enhanced by GAE and GAW. In contrast to the evident renal toxicity of allopurinol, GAE and GAW did not show a distinct renal toxicity. Almost no suppressing effect was observed on the XOD activities. However, compared to the hyperuricemia control, OAT1 was elevated remarkably in mice drugged with GAE and GAW, while GLUT9 was significantly decreased. Similar to benzbromarone, GAE decreased the URAT1 protein levels significantly ( < 0.01), while GAW did not display a similar effect. GAE and GAW downregulated the level of CNT2 proteins in the gastrointestinal tract of hyperuricemia mice. Thus, produced outstanding hypouricemic effects, mediated by renal OAT1, GLUT9, and URAT1 and gastrointestinal CNT2 that might elevate urine uric secretions and decline in the absorption of purine in the gastrointestinal tracts. showed little negative influence on inner organs. By docking screening, four top-ranked compounds were identified that necessitated further investigation. potassium oxonate, hypoxanthine, allopurinol, benzbromarone.
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http://dx.doi.org/10.3389/fphar.2017.00996DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775298PMC
January 2018

Protective Effect of Pogostone on 2,4,6-Trinitrobenzenesulfonic Acid-Induced Experimental Colitis via Inhibition of T Helper Cell.

Front Pharmacol 2017 17;8:829. Epub 2017 Nov 17.

Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou, China.

Inflammatory bowel disease (IBD) is a chronic immune-related disease mainly caused by the disequilibrium of T helper (Th) cell paradigm? Pogostone (PO) is one of the major chemical constituents of (Blanco) Benth. The present study aims to investigate the potential benefit of PO against IBD in a 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis model. PO treatment by enema significantly brought down the disease activity index (DAI) of the TNBS-challenged rats, which was manifested by the ameliorated inflammatory features including ulceration, adhesion, and edema. Hematoxylin-eosin (HE) staining and immunohistochemistry analysis showed that PO effectively relived colon damage by restoring epithelium, and more importantly, by inhibiting the infiltration of pro-inflammatory Th1 and Th17 cells in the colon. Additionally, PO inhibited the activity of myeloperoxidase and secretion of inflammatory cytokines including IFN-γ, IL-12p70, IL-17A, and IL-10. Together with our previous findings, the present data indicated that the anti-IBD effect of PO probably related to its direct inhibition on Th cell proliferation and suppression of the cytokines secretion. These results highlighted the potential of PO as a promising candidate to relieve IBD.
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http://dx.doi.org/10.3389/fphar.2017.00829DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5699238PMC
November 2017

Anti-tumor and Anti-angiogenic Ergosterols from .

Front Chem 2017 30;5:85. Epub 2017 Oct 30.

Guangdong Institute of Microbiology, State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, Guangdong Open Laboratory of Applied Microbiology, Guangzhou, China.

This study was carried out to isolate chemical constituents from the lipid enriched fraction of extract and to evaluate their anti-proliferative effect on tumor cells and human umbilical vein endothelial cells (HUVECs). Ergosterol derivatives (-) were isolated and purified from the lipid enriched fraction of . Their chemical structures were established by spectroscopic analyses or by comparison of mass and NMR spectral data with those reported previously. Amongst, compound was purified and identified as a new one. All the compounds were evaluated for their anti-proliferative effect on human tumor cells and HUVECs . Compounds displayed inhibitory activity against two types of human tumor cells and HUVECs, which indicated that these four compounds had both anti-tumor and anti-angiogenesis activities. Compound had significant selective inhibition against two tumor cell lines, while exhibited selective inhibition against HUVECs. The structure-activity relationships for inhibiting human HepG2 cells were revealed by 3D-QASR. Ergosterol content in different parts of the raw material and products of was quantified. This study provides a basis for further development and utilization of ergosterol derivatives as natural nutraceuticals and functional food ingredients, or as source of new potential antitumor or anti-angiogenesis chemotherapy agent.
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http://dx.doi.org/10.3389/fchem.2017.00085DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5670154PMC
October 2017

T cell inhibition by pogostone from Pogostemon cablin (Blanco) Benth: In vitro and in vivo immunosuppressive analysis.

Mol Med Rep 2017 Oct 2;16(4):4511-4520. Epub 2017 Aug 2.

Guangdong Provincial Key Laboratory of New Drug Development and Research of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.

Various plant-derived compounds exhibit immunosuppressive activity in pre‑clinical investigations, suggesting that they may serve as natural alternatives for the prevention of inflammatory disorders and autoimmune diseases. The aim of the current study was to explore the immunosuppressive potential of pogostone (PO) derived from Pogostemon cablin (Blanco) Benth. Carboxyfluorescein diacetate succinimidyl ester‑labeled cell tracking demonstrated that PO (20‑80 µM) inhibited Concanavalin A (ConA)‑stimulated lymphocyte proliferation, which was mediated by G0/G1 phase arrest and accompanied by significant decreases in the expression of CD69 (early‑stage activation marker) and CD25 (mid‑stage activation marker) in T cells, as indicated by flow cytometry analysis. Furthermore, the proliferation blocking ability of PO (5‑80 µM) was not associated with cytotoxicity in normal lymphocytes or apoptosis in ConA‑stimulated lymphocytes. The inflammatory cytokine profile determination using a cytometric beads assay revealed that PO inhibited release of anti‑inflammatory interleukin (IL)‑10 and pro‑inflammatory IL‑6 from the stimulated lymphocytes. Furthermore, PO (10, 20 or 40 mg/kg) ameliorated the T‑cell mediated delayed type hypersensitivity response in Balb/c mice by reducing leukocyte infiltration and tissue edema, providing a further validation of the direct immunosuppressive activity of PO. Together, the present data suggest that PO would suppress T cell response via a direct non‑cytotoxic inactivation at the early stage, accompanied by regulation of the inflammatory cytokine profile, which highlights clinical implications for treatment of immune-based disorders.
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http://dx.doi.org/10.3892/mmr.2017.7147DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647011PMC
October 2017

Immunomodulatory Activities of a Fungal Protein Extracted from through Regulating the Gut Microbiota.

Front Immunol 2017 12;8:666. Epub 2017 Jun 12.

State Key Laboratory of Applied Microbiology South China, Guangdong Institute of Microbiology, Guangzhou, China.

A single-band protein (HEP3) was isolated from using a chemical separation combined with pharmacodynamic evaluation methods. This protein exhibited immunomodulatory activity in lipopolysaccharide-activated RAW 264.7 macrophages by decreasing the overproduction of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6, and downregulating the expression of inducible nitric oxide synthase and nuclear factor-κB p65. Further researches revealed that HEP3 could improve the immune system regulating the composition and metabolism of gut microbiota to activate the proliferation and differentiation of T cells, stimulate the intestinal antigen-presenting cells in high-dose cyclophosphamide-induced immunotoxicity in mice, and play a prebiotic role in the case of excessive antibiotics in inflammatory bowel disease model mice. Aided experiments also showed that HEP3 could be used as an antitumor immune inhibitor in tumor-burdened mice. The results of the present study suggested that fungal protein from could be used as a drug or functional food ingredient for immunotherapy because of its immunomodulatory activities.
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http://dx.doi.org/10.3389/fimmu.2017.00666DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5492111PMC
June 2017

Cytotoxic lanostane-type triterpenoids from the fruiting bodies of Ganoderma lucidum and their structure-activity relationships.

Oncotarget 2017 Feb;8(6):10071-10084

Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, Canada.

We conducted a study of Ganoderma lucidum metabolites and isolated 35 lanostane-type triterpenoids, including 5 new ganoderols (1-5). By spectroscopy, we compared the structures of these compounds with known related compounds in this group. All of the isolated compounds were assayed for their effect against the human breast carcinoma cell line MDA-MB-231 and hepatocellular carcinoma cell line HepG2. Corresponding three-dimensional quantitative structure-activity relationship (3D-QSAR) models were built and analyzed using Discovery Studio. These results provide further evidence for anti-cancer constituents within Ganoderma lucidum, and may provide a theoretical foundation for designing novel therapeutic compounds.
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http://dx.doi.org/10.18632/oncotarget.14336DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354642PMC
February 2017

Actions of water extract from Cordyceps militaris in hyperuricemic mice induced by potassium oxonate combined with hypoxanthine.

J Ethnopharmacol 2016 Dec 4;194:403-411. Epub 2016 Oct 4.

State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application and Guangdong Open Laboratory of Applied Microbiology, Guangdong Institute of Microbiology, Guangzhou 510070, China; Guangdong Yuewei Edible Fungi Technology Co., Guangzhou 510663, China.

Ethnopharmacological Relevance: Cordyceps militaris was recorded in the classic traditional Chinese medicine book with the main functions of "protecting liver and enhancing kidney functions", influencing serum uric acid levels.

Aim Of Study: The aim is to investigate the hypouricemic effects and possible mechanism of C. militaris in hyperuricemic mice.

Materials And Methods: A water extract (WECM) was prepared by decocting C. militaris directly at 80 °C in water bath, followed by lyophilization. WECM at 50, 100 and 200mg/kg was orally administered to hyperuricemic mice induced by potassium oxonate and hypoxanthine combinedly and allopurinol (5mg/kg) was served as a positive control.

Results: WECM exhibited excellent hypouricemic activity, which could decrease the serum uric acid levels of the hyperuricemic mice (306μmol/L) to 189, 184 and 162μmol/L at different doses respectively (P<0.01), approaching the levels of normal mice (184μmol/L). The urate transporter 1 (URAT1) protein levels of kidney at different doses of WECM were 28.15, 17.43, 9.03pg/mL respectively, much lower than that in the hyperuricemia group (93.45pg/mL, P<0.01); and suggested WECM may interact with URAT1. Docking simulations using modeled structure of URAT1 suggested that LYS145, ARG325, ARG477 and ASP168 of URAT1 are key functional residues of URAT1. Four active compounds in C. militaris were identified and their interaction energies with target were estimated between -200 and -400kcal/mol.

Conclusions: These findings suggested that C. militaris produced significant hypouricemic actions and the hypouricemic effects of WECM may be attributed to the inhibitive effect of WECM on URAT1 protein levels. The results of blood urine nitrogen and serum creatinine levels and liver, kidney and spleen coefficients showed that WECM have no negative impacts on liver, renal and spleen functions. The screened four active compounds using molecular docking method deserve further investigation in other work.
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http://dx.doi.org/10.1016/j.jep.2016.10.001DOI Listing
December 2016

Protective effects of apigenin against 1-methyl-4-phenylpyridinium ion‑induced neurotoxicity in PC12 cells.

Int J Mol Med 2015 Mar 30;35(3):739-46. Epub 2014 Dec 30.

School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, P.R. China.

Parkinson's disease is recognized as the second most common neurodegenerative disorder after Alzheimer's disease, characterized by the loss of dopominergic neurons in the substantia nigra pars compacta and can be experimentally mimicked by the use of the neurotoxin, 1‑methyl‑4‑phenylpyridinium ion (MPP(+)), in in vitro models. In this study, we investigated the potential protective effects of apigenin (AP), galangin and genkwanin, naturally occurring plant flavonoids, on the MPP(+)‑induced cytotoxicity in cultured rat adrenal pheochromocytoma cells (PC12 cells). The PC12 cells were pre-treated with various concentrations of the test compounds for 4 h, followed by the challenge with 1,000 µM MPP(+) for 48 h. We found that only pre-treatment with AP (3, 6 and 12 µM) before injury significantly increased cell viability, decreased the release of lactate dehydrogenase, reduced the level of intracellular reactive oxygen species and elevated mitochondrial membrane potential in the MPP(+)‑treated PC12 cells. In addition, AP markedly suppressed the increased rate of apoptosis and the reduced Bcl‑2/Bax ratio induced by MPP(+) in the PC12 cells. Taken together, the findings of this study demonstrate that AP exerts neuroprotective effects against MPP(+)‑induced neurotoxicity in PC12 cells, at least in part, through the inhibition of oxidative damage and the suppression of apoptosis through the mitochondrial pathway.
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http://dx.doi.org/10.3892/ijmm.2014.2056DOI Listing
March 2015

Apigenin mediated protection of OGD-evoked neuron-like injury in differentiated PC12 cells.

Neurochem Res 2014 Nov 11;39(11):2197-210. Epub 2014 Sep 11.

The Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, People's Republic of China.

Ischemic stroke has been confirmed to cause neuronal injury due to its insufficient supply of glucose and oxygen to brain tissue. Previous research has shown that oxidative stress, a result of excessive accumulation of reactive oxygen species (ROS), relates to pathophysiology of ischemic stroke, and causes oxidative damage to biomolecules, eventually leading to programmed cell death. Meanwhile, apigenin has been shown to exhibit antioxidant, anti-inflammatory, anti-cancer properties and neuroprotective action. Hence, this study was to investigate the potential mechanisms underlying the neural protection of apigenin on oxygen and glucose deprivation/reperfusion (OGD/R) induced neuronal injury in differentiated PC12 cells. Cells were pretreated with apigenin for 6 h, and then subjected to OGD for 12 h followed by reperfusion for 24 h. The results showed that OGD/R significantly decreased cell viability, mitochondrial membrane potential, mRNA levels of antioxidant and detoxifying enzymes and Nrf2 protein expression, while elevated the release of LDH, cell apoptosis, intracellular ROS level, P53 protein expression and upregulated its downstream genes in PC12 cells. However, apigenin effectively inhibited these undesirable changes induced by OGD/R. Our findings demonstrate that this compound attenuates OGD/R induced neuronal injury mainly by virtue of its anti-apoptosis and antioxidative properties via affecting the expression of Nrf2 and P53, and their downstream target gene transcription.
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http://dx.doi.org/10.1007/s11064-014-1421-0DOI Listing
November 2014

Role of CD8(+) regulatory T cells in organ transplantation.

Burns Trauma 2014 26;2(1):18-23. Epub 2014 Jan 26.

Center for Regenerative and Translational Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangdong Provincial Hospital of Chinese Medicine and Guangzhou University of Chinese Medicine School of Chinese Material Medica, Guangzhou, Guangdong, China.

CD8(+) T cells are regulatory T cells (Tregs) that suppress both alloimmunity and autoimmunity in many animal models. This class of regulatory cells includes the CD8(+)CD28(-), CD8(+)CD103(+), CD8(+)FoxP3(+) and CD8(+)CD122(+) subsets. The mechanisms of action of these regulatory cells are not fully understood; however, the secretion of immunosuppressive cytokines, such as interleukin (IL)-4, IL-10 and transforming growth factor beta (TGF-β) as well as the direct killing of target cells via Fas L/Fas and the perforin/granzyme B pathways have been demonstrated in various models. Further studies are necessary to fully understand the mechanisms underlying the suppressive effects of Tregs and to provide experimental support for potential clinical trials. We recently observed that CD8(+)CD122(+) Tregs more potently suppressed allograft rejection compared to their CD4(+)CD25(+) counterparts, supporting the hypothesis that CD8(+) Tregs may represent a new and promising Treg family that can be targeted to prevent allograft rejection in the clinic. In this review, we summarize the progress in the field during the past 7-10 years and discuss CD8(+) Treg phenotypes, mechanisms of action, and their potential clinical applications; particularly in composite tissue transplants in burn and trauma patients.
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http://dx.doi.org/10.4103/2321-3868.126086DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4994507PMC
August 2016

Kinetics and mechanism study of competitive inhibition of jack-bean urease by baicalin.

ScientificWorldJournal 2013 1;2013:879501. Epub 2013 Oct 1.

School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, China.

Baicalin (BA) is the principal component of Radix Scutellariae responsible for its pharmacological activity. In this study, kinetics and mechanism of inhibition by BA against jack-bean urease were investigated for its therapeutic potential. It was revealed that the IC₅₀ of BA against jack-bean urease was 2.74 ± 0.51 mM, which was proved to be a competitive and concentration-dependent inhibition with slow-binding progress curves. The rapid formation of initial BA-urease complex with an inhibition constant of K(i) = 3.89 × 10⁻³ mM was followed by a slow isomerization into the final complex with an overall inhibition constant of K(i)* = 1.47 × 10⁻⁴ mM. High effectiveness of thiol protectors against BA inhibition indicated that the strategic role of the active-site sulfhydryl group of the urease was involved in the blocking process. Moreover, the inhibition of BA was proved to be reversible due to the fact that urease could be reactivated by dithiothreitol but not reactant dilution. Molecular docking assay suggested that BA made contacts with the important activating sulfhydryl group Cys-592 residues and restricted the mobility of the active-site flap. Taken together, it could be deduced that BA was a competitive inhibitor targeting thiol groups of urease in a slow-binding manner both reversibly and concentration-dependently, serving as a promising urease inhibitor for treatments on urease-related diseases.
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http://dx.doi.org/10.1155/2013/879501DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3807542PMC
June 2014

[Fingerprint research and multi-component quantitative analysis of Kumu injection by HPLC].

Zhongguo Zhong Yao Za Zhi 2011 Jul;36(13):1739-43

New Drug R&D Department, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.

Objective: To establish the HPLC chromatographic fingerprint of Kumu injection and to simultaneously determine the contents of three beta-carboline alkaloids, comprehensively evaluating the immanent quality of Kumu injection.

Method: The chromatographic analysis was performed on a Phenomenex Gemini C18 ( 4.6 mm x 250 mm, 5 microm) column with the gradient elution solvent system composed of methanol and 30 mmol x L(-1) aqueous ammonium acetate (adjusted with glacial acetic acid to pH 4.5). Similarity evaluation system for chromatographic fingerprint of traditional Chinese medicine (2004 A) was used in data analysis.

Result: Sixteen co-possessing peaks were selected as the fingerprints of Kumu injection, and 7 peaks were identified by chemical reference substances. There were good similarities between the standard fingerprint chromatogram and each fingerprint chromatogram from the eleven samples for their similarity coefficients were not less than 0.9. Three kinds of beta-carboline alkaloids were separated well. The correlation coefficients were 0.999 9. The linear ranges of three components were 0.020 0-0.300 0, 0.102 0-1.530 0, 0.015 2-0. 228 0 microg, respectively, and the average recoveries ranged were from 99.5% to 102%.

Conclusion: The method of fingerprint combined with quantitative analysis is sensitive, selective, and provide scientific basis for quality control of Kumu Injection.
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July 2011
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