Publications by authors named "Hyun-Ji Oh"

18 Publications

  • Page 1 of 1

Dysfunction of B Cell Leading to Failure of Immunoglobulin Response Is Ameliorated by Dietary Silk Peptide in 14-Month-Old C57BL/6 Mice.

Front Nutr 2020 19;7:583186. Epub 2020 Nov 19.

Department of Biomedical Sciences, CHA University, Pocheon, South Korea.

Anti-aging research suggests that immunosenescent cells can play deleterious roles in the immune system. Here, young (2 months old) and old (14 months old) C57BL/6 mice received a daily oral dose (100 or 750 mg/kg/day) of acid-hydrolyzed silk peptide (SP) for a period of 5 weeks. Mouse spleen, lymph node, and serum were analyzed to determine the immune homeostasis of SP by flow cytometry, Western blotting, ELISA, and qRT-PCR. The results suggest that SP ameliorates age-related dysfunction of T and B cells. Amelioration of B cell dysfunction improved the immunoglobulin response in aged mice. Taken together, the results suggest that SP restores immune homeostasis with respect to immunosenescent cells.
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http://dx.doi.org/10.3389/fnut.2020.583186DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7710868PMC
November 2020

The Gintonin-Enriched Fraction of Ginseng Regulates Lipid Metabolism and Browning via the cAMP-Protein Kinase a Signaling Pathway in Mice White Adipocytes.

Biomolecules 2020 07 15;10(7). Epub 2020 Jul 15.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyonggi-do 13488, Korea.

Obesity is a major health concern and is becoming an increasingly serious societal problem worldwide. The browning of white adipocytes has received considerable attention because of its potential protective effect against obesity-related metabolic disease. The gintonin-enriched fraction (GEF) is a non-saponin, glycolipoprotein component of ginseng that is known to have neuroprotective and anti-inflammatory effects. However, the anti-obesity and browning effects of GEF have not been explored to date. Therefore, we aimed to determine whether GEF has a preventive effect against obesity. We differentiated 3T3-L1 cells and mouse primary subcutaneous adipocytes for 8 days in the presence or absence of GEF, and then measured the expression of intermediates in signaling pathways that regulate triglyceride (TG) synthesis and browning by Western blotting and immunofluorescence analysis. We found that GEF reduced lipid accumulation by reducing the expression of pro-adipogenic and lipogenic factors, and increased lipolysis and thermogenesis, which may be mediated by an increase in the phosphorylation of protein kinase A. These findings suggest that GEF may induce fat metabolism and energy expenditure in white adipocytes and therefore may represent a potential treatment for obesity.
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http://dx.doi.org/10.3390/biom10071048DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7407952PMC
July 2020

Coreolanceolins A-E, New Flavanones from the Flowers of and Their Antioxidant and Anti-inflammatory Effects.

Antioxidants (Basel) 2020 Jun 19;9(6). Epub 2020 Jun 19.

Graduate School of Biotechnology and Department of Oriental Medicinal Biotechnology, Kyung Hee University, Yongin 17104, Korea.

(1) Background: Many flavonoids derived from natural sources have been reported to exhibit antioxidant and anti-inflammatory effects. Our preliminary study suggested that flowers (CLFs) include high flavonoid content; (2) Methods: CLFs were extracted in 80% (v/v) aqueous methanol and fractionated into ethyl acetate, -butanol, and water fractions. Repeated column chromatographies for the organic fractions led to the isolation of seven flavanones. Quantitative analysis of the flavanones was carried out using reversed-phase high-performance liquid chromatography. All flavanones were evaluated for their antioxidant and pro-inflammatory inhibition effects; (3) Results: Spectroscopic analyses revealed the chemical structure of five new flavanones, coreolanceolins A-E, and two known ones. The content of the seven flavanones in extracts were determined from 0.8 ± 0.1 to 38.8 ± 0.3 mg/g. All flavanones showed radical scavenging activities (respectively 104.3 ± 1.9 to 20.5 ± 0.3 mg vitamin C equivalents (VCE)/100 mg and 1278.6 ± 26.8 to 325.6 ± 0.2 mg VCE/100 mg) in the DPPH and 2,2'-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assays and recovery activities in Caco-2 (59.7 to 41.1%), RAW264.7 (87.8 to 56.0%), and PC-12 (100.5 to 69.9%) cells against reactive oxygen species. Furthermore, all flavanones suppressed nitric oxide production (99.5% to 37.3%) and reduced iNOS and COX-2 expression in lipopolysaccharide-treated RAW 264.7 cells; (4) Conclusions: Five new and two known flavanones were isolated from CLF, and most of them showed high antioxidant and pro-inflammatory inhibition effects.
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http://dx.doi.org/10.3390/antiox9060539DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7346140PMC
June 2020

Dietary Silk Peptide Inhibits LPS-Induced Inflammatory Responses by Modulating Toll-Like Receptor 4 (TLR4) Signaling.

Biomolecules 2020 05 15;10(5). Epub 2020 May 15.

Department of Biomedical Sciences, CHA University, Gyeonggi-do 13488, Korea.

Acid-hydrolyzed silk peptide (SP) is a valuable material that has been used traditionally to treat various diseases, however, the mechanism by which it affects inflammatory responses is unknown. To examine the effects of SP on inflammatory responses, we used macrophages as a vehicle for examining signaling via toll-like receptor 4 (TLR4), which plays an important role in innate immune responses to pathogenic infections and pathogen-derived molecules such as lipopolysaccharide (LPS). We then confirmed the anti-inflammatory effects of SP by examining lymph node, spleen, and serum samples from C57BL/6 mice injected with LPS. We also used LPS-induced bone marrow-derived macrophages and RAW264.7 cells (a murine macrophage cell line) to identify the mechanism by which SP modulates immune responses via the TLR4 signaling pathway. In addition, we showed that SP prevents LPS-induced production of nitric oxide and reactive oxygen species. In summary, SP inhibits LPS-induced inflammatory responses by modulating the TLR4 signaling pathway.
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http://dx.doi.org/10.3390/biom10050771DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7277379PMC
May 2020

Korean Red Ginseng Suppresses the Expression of Oxidative Stress Response and NLRP3 Inflammasome Genes in Aged C57BL/6 Mouse Ovaries.

Foods 2020 Apr 22;9(4). Epub 2020 Apr 22.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyonggi 13488, Korea.

Female infertility and subfertility have been increasing in prevalence worldwide. One contributing factor is ovarian function, which is highly age-dependent. Korean red ginseng is widely used as an herbal medicine and has many beneficial properties. We aimed to determine the effect of the Korean red ginseng saponin fraction (KRGSF) on ovarian function in female C57BL/6 mice. Ovaries were isolated from 6- and 12-month-old female mice and treated with KRGSF, and then RNA was extracted and microarray analysis was performed. The expression of key genes was subsequently verified using quantitative RT-PCR. Aging markedly increased the expression of genes encoding oxidative stress factors and NLRP3 inflammasome components, but the expression of these genes was significantly reduced by KRGSF treatment. Thus, the reduction in ovarian health with age is associated with greater oxidative stress response and inflammation, but KRGSF treatment may limit these age-related changes.
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http://dx.doi.org/10.3390/foods9040526DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231237PMC
April 2020

Extract Suppresses Lipid Accumulation by Promoting Lipolysis and Adipose Browning in High-Fat Diet-Induced Obese Male Mice.

Cells 2020 04 2;9(4). Epub 2020 Apr 2.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Gyeonggi 13488, Korea.

Obesity develops due to an energy imbalance and manifests as the storage of excess triglyceride (TG) in white adipose tissue (WAT). Recent studies have determined that edible natural materials can reduce lipid accumulation and promote browning in WAT. We aimed to determine whether extract (ESE) would increase the energy expenditure in high-fat diet (HFD)-induced obese mice and 3T3-L1 cells by upregulating lipolysis and browning. ESE is an edible brown marine alga that belongs to the family Laminariaceae and contains dieckol, a phlorotannin. We report that ESE inhibits body mass gain by regulating the expression of proteins involved in adipogenesis and lipogenesis. In addition, ESE activates protein kinase A (PKA) and increases the expression of lipolytic enzymes including adipose triglyceride lipase (ATGL), phosphorylated hormone-sensitive lipase (p-HSL), and monoacylglycerol lipase (MGL) and also thermogenic genes, such as carnitine palmitoyltransferase 1 (CPT1), PR domain-containing 16 (PRDM16), and uncoupling protein 1 (UCP1). These findings indicate that ESE may represent a promising natural means of preventing obesity and obesity-related metabolic diseases.
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http://dx.doi.org/10.3390/cells9040871DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226821PMC
April 2020

Gomisin N from Ameliorates Lipid Accumulation and Induces a Brown Fat-Like Phenotype through AMP-Activated Protein Kinase in 3T3-L1 Adipocytes.

Int J Mol Sci 2020 Mar 20;21(6). Epub 2020 Mar 20.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyonggi-do 13488, Korea.

Obesity results from an imbalance between energy intake and energy expenditure, in which excess fat is stored as triglycerides (TGs) in white adipocytes. Recent studies have explored the anti-obesity effects of certain edible phytochemicals, which suppress TG accumulation and stimulate a brown adipocyte-like phenotype in white adipocytes. Gomisin N (GN) is an important bioactive component of , a woody plant endemic to Asia. GN has antioxidant, anti-inflammatory and hepatoprotective effects in vivo and in vitro. However, the anti-obesity effects of GN in lipid metabolism and adipocyte browning have not yet been investigated. In the present study, we aimed to determine whether GN suppresses lipid accumulation and regulates energy metabolism, potentially via AMP-activated protein kinase (AMPK), in 3T3-L1 adipocytes. Our findings demonstrate that GN inhibited adipogenesis and lipogenesis in adipocyte differentiation. Also, GN not only increased the expression of thermogenic factors, including uncoupling protein 1 (UCP1), but also enhanced fatty acid oxidation (FAO) in 3T3-L1 cells. Therefore, GN may have a therapeutic benefit as a promising natural agent to combat obesity.
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http://dx.doi.org/10.3390/ijms21062153DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139380PMC
March 2020

Gintonin-Enriched Fraction Suppresses Heat Stress-Induced Inflammation Through LPA Receptor.

Molecules 2020 Feb 25;25(5). Epub 2020 Feb 25.

Department of Biomedical Sciences, CHA University, Seongnam-si 13488, Gyeonggi-do, Korea.

Heat stress can be caused by various environmental factors. When exposed to heat stress, oxidative stress and inflammatory reaction occur due to an increase of reactive oxygen species (ROS) in the body. In particular, inflammatory responses induced by heat stress are common in muscle cells, which are the most exposed to heat stress and directly affected. Gintonin-Enriched Fraction (GEF) is a non-saponin component of ginseng, a glycolipoprotein. It is known that it has excellent neuroprotective effects, therefore, we aimed to confirm the protective effect against heat stress by using GEF. C2C12 cells were exposed to high temperature stress for 1, 12 and 15 h, and the expression of signals was analyzed over time. Changes in the expression of the factors that were observed under heat stress were confirmed at the protein level. Exposure to heat stress increases phosphorylation of p38 and extracellular signal-regulated kinase (ERK) and increases expression of inflammatory factors such as NLRP3 inflammasome through lysophosphatidic acid (LPA) receptor. Activated inflammatory signals also increase the secretion of inflammatory cytokines such as interleukin 6 (IL-6) and interleukin 18 (IL-18). Also, expression of glutathione reductase (GR) and catalase related to oxidative stress is increased. However, it was confirmed that the changes due to the heat stress were suppressed by the GEF treatment. Therefore, we suggest that GEF helps to protect heat stress in muscle cell and prevent tissue damage by oxidative stress and inflammation.
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http://dx.doi.org/10.3390/molecules25051019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7179209PMC
February 2020

Effect of Dietary Silk Peptide on Obesity, Hyperglycemia, and Skeletal Muscle Regeneration in High-Fat Diet-Fed Mice.

Cells 2020 02 6;9(2). Epub 2020 Feb 6.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyonggi-do 13488, Korea.

Obesity is associated with excess body fat accumulation that can cause hyperglycemia and reduce skeletal muscle function and strength, which characterize the development of sarcopenic obesity. In this study, we aimed to determine the mechanism whereby acid-hydrolyzed silk peptide (SP) prevents high-fat diet (HFD)-induced obesity and whether it regulates glucose uptake and muscle differentiation using in vivo and in vitro approaches. Our findings demonstrate that SP inhibits body mass gain and the expression of adipogenic transcription factors in visceral adipose tissue (VAT). SP also had an anti-diabetic effect in VAT and skeletal muscle because it upregulated glucose transporter type 4 (GLUT4) and uncoupling protein 3 (UCP3) expression. Furthermore, SP reduced ubiquitin proteasome and promoted myoblast determination protein 1 (MyoD)/myogenic factor 4 (myogenin) expression, implying that it may have potential for the treatment of obesity-induced hyperglycemia and obesity-associated sarcopenia.
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http://dx.doi.org/10.3390/cells9020377DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072146PMC
February 2020

Spirulina maxima extract prevents activation of the NLRP3 inflammasome by inhibiting ERK signaling.

Sci Rep 2020 02 7;10(1):2075. Epub 2020 Feb 7.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Pangyo-ro 335, Bundang-gu, Seongnam-si, Gyeonggi-do, 13488, Republic of Korea.

The blue-green alga Spirulina maxima is a microscopic filamentous cyanobacterium. Spirulina was recently reported to elicit beneficial effects such as reducing cholesterol and inducing weight loss; however, its effects on inflammation are unknown. To determine the effect of S. maxima extract (SME) on innate immunity, we investigated the NLRP3 inflammasome activation, which is a multiprotein scaffolding complex that plays important roles in innate immune responses to many pathogenic infections in macrophages. SME suppressed lipopolysaccharide (LPS)-induced upregulation of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-12, IL-1β, and IL-18 in RAW264.7 cells. In addition, SME attenuated LPS-induced NLRP3 inflammasome activation, and thus pro-IL-1β could not be cleaved to IL-1β by activated caspase-1, which is activated by the NLRP3 inflammasome in RAW264.7 cells. Moreover, SME inhibited LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK) in RAW264.7 cells, and attenuated the generation of ERK1 induced-reactive oxygen species (ROS), resulting in decreased expression of NF-κB. These findings suggest that SME suppresses the effects of the NLRP3 inflammasome via regulation of extracellular signal-regulated kinase (ERK). In summary, we demonstrated that SME prevents activation of the NLRP3 inflammasome by inhibiting ERK signaling.
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http://dx.doi.org/10.1038/s41598-020-58896-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7005707PMC
February 2020

Anti-Inflammatory Effect of Flavonoids from L. Flowers.

J Microbiol Biotechnol 2020 Feb;30(2):163-171

Graduate School of Biotechnology and Department of Oriental Medicinal Biotechnology, Kyung Hee University, Yongin 17104, Republic of Korea.

L. (Solanaceae), commonly known as "angel's trumpet," is widely grown in North America, Africa, Australia, and Asia. It has been mainly used for ornamental purposes as well as analgesic, anti-rheumatic, vulnerary, decongestant, and anti-spasmodic materials. is also reported to show anti-cholinergic activity, for which many alkaloids were reported to be principally responsible. However, to the best of our knowledge, a phytochemical study of flowers has not yet been performed. Four flavonol glycosides () and one dihydroflavanol () were for the first time isolated from flowers in this study. The flavonoids showed significant antioxidant capacities, suppressed nitric oxide production in lipopolysaccharide (LPS)-treated RAW 264.7 cells, and reduced inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) protein production increased by LPS treatment. The contents of compounds in -BuOH fraction were determined to be 3.8 ± 0.9%, 2.2 ± 0.5%, 20.3 ± 1.1%, and 2.3 ± 0.4%, respectively, and that of compound 5 in EtOAc fraction was determined to be 12.7 ± 0.7%, by HPLC experiment. These results suggest that flavonol glycosides () and dihydroflavanol () can serve as index components of flowers in standardizing anti-inflammatory materials.
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http://dx.doi.org/10.4014/jmb.1907.07058DOI Listing
February 2020

Dietary Silk Peptide Prevents High-Fat Diet-Induced Obesity and Promotes Adipose Browning by Activating AMP-Activated Protein Kinase in Mice.

Nutrients 2020 Jan 13;12(1). Epub 2020 Jan 13.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam 13488, Korea.

Obesity is associated with metabolic syndrome and other chronic diseases, and is caused when the energy intake is greater than the energy expenditure. We aimed to determine the mechanism whereby acid-hydrolyzed silk peptide (SP) prevents high-fat diet-induced obesity, and whether it induces browning and fatty acid oxidation (FAO) in white adipose tissue (WAT), using in vivo and ex vivo approaches. We determined the effects of dietary SP in high-fat diet-fed obese mice. The expression of adipose tissue-specific genes was quantified by western blotting, qRT-PCR, and immunofluorescence analysis. We also investigated whether SP directly induces browning in primarily subcutaneous WAT-derived adipocytes. Our findings demonstrate that SP has a browning effect in WAT by upregulating AMP-activated Protein Kinase (AMPK) phosphorylation and uncoupling protein 1 (UCP1) expression. SP also suppresses adipogenesis and promotes FAO, implying that it may have potential as an anti-obesity drug.
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http://dx.doi.org/10.3390/nu12010201DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7019986PMC
January 2020

Cardamonin suppresses lipogenesis by activating protein kinase A-mediated browning of 3T3-L1 cells.

Phytomedicine 2019 Dec 3;65:153064. Epub 2019 Aug 3.

Department of Food Science and Biotechnology, College of Life Science, CHA University, Seongnam, Kyeonggi 13488, South Korea. Electronic address:

Background: Obesity develops when dietary energy intake exceeds energy expenditure, and can be associated with metabolic syndrome. Recent studies have shown that dietary phytochemicals can promote energy expenditure by inducing the browning of white adipose tissue (WAT).

Purpose: This study investigated whether cardamonin induces the browning of 3T3-L1 adipocytes through the activation of protein kinase A (PKA).

Methods: Anti-obesity potential of cardamonin was evaluated in 3T3-L1 adipocytes. Adipocyte-specific genes were observed using western blot, qPCR analysis and immunocytochemistry.

Results: Cardamonin treatment inhibited lipid droplet accumulation and reduced the expression of the adipogenic proteins C/EBPα and FABP4, and the lipogenic proteins LPAATθ, lipin 1, DGAT1, SREBP1, and FAS. Cardamonin also induced the expression of the browning marker genes PRDM16, PGC1α, and UCP1 at the mRNA and protein levels, and induced mRNA expression of CD137, a key marker of beige adipocytes. It also increased the expression of the β-oxidation genes CPT1 and PPARα at the mRNA and protein levels. In addition, cardamonin increased PKA phosphorylation and the mRNA and protein expression of the downstream lipolytic enzymes adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL).

Conclusion: Our findings demonstrate novel effects of cardamonin to stimulate adipocyte browning, suppress lipogenesis, and promote lipolysis, implying it may have potential as an anti-obesity agent.
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http://dx.doi.org/10.1016/j.phymed.2019.153064DOI Listing
December 2019

Magnolol Suppresses TGF-β-Induced Epithelial-to-Mesenchymal Transition in Human Colorectal Cancer Cells.

Front Oncol 2019 1;9:752. Epub 2019 Oct 1.

Department of Food Science and Biotechnology, College of Biomedical Sciences, CHA University, Seongnam, South Korea.

Tumor metastasis is the end state of a multistep process that includes dissemination of tumor cells to distant organs and requires tumor cells to adapt to different tissue microenvironments. During metastasis, tumor cells undergo a morphological change known as transdifferentiation or the epithelial-to-mesenchymal transition (EMT). In normal embryonic development, the EMT occurs in the context of morphogenesis in a variety of tissues. Over the course of this process, epithelial cells lose their cell-cell adhesion and polarity properties. In this study, we investigated whether magnolol could suppress the EMT in human colorectal cancer cells. To this end, we examined the epithelial markers E-cadherin, ZO-1, and claudin and the mesenchymal markers N-cadherin, TWIST1, Slug, and Snail. Magnolol effectively inhibited EMT in human colon cancer cell lines by upregulating epithelial markers and downregulating mesenchymal markers. The EMT is induced by the TGF-β signaling pathway. To determine whether magnolol disrupts TGF-β signaling, we examined several mediators of this pathway, and found that magnolol decreased the levels of phosphorylated (i.e., active) ERK, GSK3β, and Smad. We conclude that magnolol blocks migration in HCT116 cells by suppressing TGF-β signaling.
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http://dx.doi.org/10.3389/fonc.2019.00752DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6779771PMC
October 2019

Lanceoleins A-G, hydroxychalcones, from the flowers of Coreopsis lanceolata and their chemopreventive effects against human colon cancer cells.

Bioorg Chem 2019 04 4;85:274-281. Epub 2019 Jan 4.

Graduate School of Biotechnology and Department of Oriental Medicine Biotechnology, Kyung-Hee University, Yongin 17104, Republic of Korea. Electronic address:

Seven new chalcones, lanceolein A-G (compounds 5 and 7-12), as well as five known chalcones (1-4 and 6), were isolated from the methanolic extract of Coreopsis lanceolata flowers. The chemical structures of 5 and 7-12 were determined on the basis of spectroscopic data interpretation. All compounds inhibited the production of nitrite oxide (NO) induced by LPS in RAW264.7 macrophage cells. Also, compounds 1-6 showed moderated cytotoxicity against human colon cancer cell lines, while compounds 7-12 hardly showed the cytotoxicity. Especially, compounds 2, 5, and 6 exhibited a little higher cytotoxicity on HCT15 cells, with IC values of 43.7 ± 2.17 μM, 35.6 ± 0.24 μM, and 47.9 ± 1.18 μM, respectively. In the Tali assay, compounds 2 and 5 increased the numeral of apoptotic cells. These compounds also significantly promoted the expression of apoptotic proteins including PARP and caspase-3.
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http://dx.doi.org/10.1016/j.bioorg.2019.01.003DOI Listing
April 2019

Heteroleptic strontium complexes stabilized by donor-functionalized alkoxide and β-diketonate ligands.

Dalton Trans 2015 Aug;44(31):14042-53

Thin Film Materials Research Center, Korea Research Institute of Chemical Technology, P.O. Box 107, 141 Gajeong-Ro, Yuseong-Gu, Daejeon 305-600, Republic of Korea.

Heteroleptic complexes of strontium () were prepared by employing β-diketonates and donor-functionalized alkoxides as coordinating ligands. The results illustrate the effect of alkoxide substituent groups on the overall structures of the complexes. The presence of a terminal methoxy group in the alkoxide ligands leads to the formation of trimeric complexes , whereas the substituents on the amine nitrogen prove to have less influence in determining the structure. The attempts to increase steric bulkiness of the aminoalkoxide ligands by introducing ethyl groups on the amine nitrogen and to the alkoxy carbon did not lead to a structural change from the dimeric form in but resulted in structurally interesting strontium complexes. In trimeric complexes , the three strontium atoms were held together by two μ3-O bonds using alkoxide oxygen atoms and two μ2-O bonds using a combination of alkoxide and β-diketonate ligand oxygens. The strontium metal centers in these complexes exhibit seven-coordination states in and , whereas exhibits one six-coordinated and two seven-coordinated strontium metals in its structure. All of the complexes were characterized using FT-NMR, FT-IR, elemental analyses, and thermogravimetric (TG) analyses.
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http://dx.doi.org/10.1039/c5dt01356aDOI Listing
August 2015

D-glucosamine inhibits proliferation of human cancer cells through inhibition of p70S6K.

Biochem Biophys Res Commun 2007 Sep 5;360(4):840-5. Epub 2007 Jul 5.

Chronic Disease Research Center and Institute for Medical Science, School of Medicine, Keimyung University, Daegu 700-712, Republic of Korea.

Although D-glucosamine has been reported as an inhibitor of tumor growth both in vivo and in vitro, the mechanism for the anticancer effect of D-glucosamine is still unclear. Since there are several reports suggesting D-glucosamine inhibits protein synthesis, we examined whether D-glucosamine affects p70S6K activity, an important signaling molecule involved in protein translation. In the present study, we found D-glucosamine inhibited the activity of p70S6K and the proliferation of DU145 prostate cancer cells and MDA-MB-231 breast cancer cells. D-glucosamine decreased phosphorylation of p70S6K, and its downstream substrates RPS6, and eIF-4B, but not mTOR and 4EBP1 in DU145 cells, suggesting that D-glucosamine induced inhibition of p70S6K is not through the inhibition of mTOR. In addition, D-glucosamine enhanced the growth inhibitory effects of rapamycin, a specific inhibitor of mTOR. These findings suggest that D-glucosamine can inhibit growth of cancer cells through dephosphorylation of p70S6K.
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http://dx.doi.org/10.1016/j.bbrc.2007.06.137DOI Listing
September 2007

Leptomycin B-induced apoptosis is mediated through caspase activation and down-regulation of Mcl-1 and XIAP expression, but not through the generation of ROS in U937 leukemia cells.

Biochem Pharmacol 2004 Jul;68(2):263-74

Chronic Disease Research Center and Institute for Medical Science, Keimyung University School of Medicine, Jung-gu, Daegu 700-712, South Korea.

Leptomycin B (LMB), which is originally isolated from Streptomyces, possesses anti-tumor properties in vivo and in vitro. Though it was previously reported that LMB induces cell cycle arrest and p53-mediated apoptosis in certain cancer cells, however, the mechanism by which LMB induces apoptosis remains poorly understood. Here, we investigated the mechanisms of apoptosis induced by LMB in U937 cells. Treatment with LMB concentration-dependently induced cytotoxicity and apoptosis in U937 cells that correlated temporally with activation of caspases and down-regulation of Mcl-1 and XIAP. LMB did not change the expressions of Bcl-2 or Bax. A broad spectrum caspase inhibitor, z-VAD-fmk, blocked caspase-3 activation and elevated the survival in LMB-treated U937 cells, suggesting that caspase-3 activation is critical for LMB-induced apoptosis. Interestingly, Bcl-2 overexpression that blocked cytochrome c release by LMB effectively attenuated the apoptotic response to LMB, suggesting that LMB-induced apoptosis is mediated through the mitochondrial pathway. Antioxidants or antioxidant enzymes had no effects on LMB-induced apoptosis. Data of flow cytometry analysis using 2',7'-dichlorofluorescein-diacetate further revealed no reactive oxygen species (ROS) generation by LMB, indicating that apoptosis induced by LMB is ROS-independent. However, the apoptotic response to LMB was not shown in U937 cells pretreated with the sulfhydryl group-containing antioxidant N-acetylcysteine (NAC). Further analysis suggested that NAC directly binds LMB and abolishes the apoptotic effects of LMB. Collectively, these findings suggest that LMB potently induces apoptosis in U937 cells, and LMB-induced apoptosis in U937 cells is related with cytochrome c release, activation of caspases, and selective down-regulation of Mcl-1 and XIAP.
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http://dx.doi.org/10.1016/j.bcp.2004.03.007DOI Listing
July 2004