• Journal of Acupuncture Research
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• v.31 no.2
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• pp.75-85
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• 2014

Objectives : We investigated whether bee venom(BV) inhibit cell growth through enhancement of death receptor expressions in the human cervix cancer C33A cells. Methods : BV($1{\sim}5{\mu}g/ml$) inhibited the growth of cervix cancer C33A cells by the induction of apoptotic cell death in a dose dependent manner. Results : Consistent with apoptotic cell death, expression of Fas, death receptor(DR) 3, 4, 5 and 6 was increased concentration dependently in the cells. Moreover, Fas, DR3 and DR6 revealed more sensitivity to BV. Thus, We reconfirmed whether they actually play a critical role in anti-proliferation of cervix cancer C33A cells. Consecutively, expression of DR downstream pro-apoptotic proteins including caspase-8, -3, -9 was upregulated and Bax was concomitantly overwhelmed the expression of Bcl-2. NF-${\kappa}B$ were also inhibited by treatment with BV in C33A cells. Conclusions : These results suggest that BV could exert anti-tumor effect through induction of apoptotic cell death in human cervix cancer C33A cells via enhancement of death receptor expression, and that BV could be a promising agent for preventing and treating cervix cancer.

• Biomedical Science Letters
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• v.18 no.3
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• pp.307-309
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• 2012

(S)-(+)-3(3,4-dihydroxy-phenyl)-acrylic acid 2,2-dimethyl-8-oxo3,4-dihydro-2H,8H-pyrano[3,2-g]Chromen-3-yl-ester (Compound 6, C6) is synthesized from (S)-(+)-decursin and attenuates the pathophysiologic progression of asthma in a ovalbumin-induced asthmatic mouse model. In the present study, we examined the effect of C6 on spontaneous apoptosis of eosinophils and neutrophils of normal and asthmatic subjects. C6 increased the apoptosis of asthmatic eosinophils in a dose-dependent manner, but it inhibited neutrophil apoptosis. C6 has no effect on apoptosis of normal eosinophils and neutrophils. LY294002, an inhibitor of PI3K, rottlerin, an inhibitor of $PKC{\delta}$, Ro-31-8425, an inhibitor of classical PKC inhibitor, PD98059, an inhibitor of MEK, and BAY 11-7085, an inhibitor of NF-${\kappa}B$, blocked the inhibitory effect on apoptosis of asthmatic neutrophils due to C6. These results indicate that C6 may be valuable as a therapeutic agent for the treatment of asthma.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5619-5625
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• 2012

Gastric carcinoma is a leading cause of cancer death in the world and multi-drug resistance (MDR) is an essential aspect of gastric carcinoma chemotherapy failure. Recent studies have shown that integrin-linked kinase (ILK) is involved in metastasis of human tumors, expression silencing of ILK inhibiting the metastasis of several types of cultured human cancer cells. However, the role and potential mechanism of ILK to reverse the multi-drug resistance in human gastric carcinoma is not fully clear. In this report, we focused on roles of expression silencing of ILK in multi-drug resistance reversal of human gastric carcinoma SGC7901/DDP cells, including increased drug sensitivity to cisplatin, cell apoptosis rates, and intracellular accumulation of Rhodamine-123, and decreased mRNA and protein expression of multi-drug resistance gene (MDR1), multi-drug resistance-associated protein (MRP1), excision repair cross-complementing gene 1 (ERCC1), glutathione S-transferase -${\pi}$ (GST-${\pi}$) and RhoE, and transcriptional activation of AP-1 and NF-${\kappa}B$ in ILK silenced SGC7901/DDP cells. We also found that there was a decreased level of p-Akt and p-ERK. The results indicated that ILK might be used as a potential therapeutic strategy to combat multi-drug resistance through blocking PI3K-Akt and MAPK-ERK pathways in human gastric carcinoma.

• Biomedical Science Letters
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• v.23 no.2
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• pp.104-110
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• 2017

Inflammation is a pathophysiological process that is known to be involved in numerous diseases. Microbial infection or tissue injury activates inflammatory responses, resulting in the induction of proinflammatory proteins including inducible nitric oxide synthase (iNOS). Aster yomena is used in traditional Korean remedies. Here, we investigated the effects of ethanol extracts of Aster yomena (EAY) on the expression of iNOS induced by ovalbumin (OVA), one of the major egg allergens, or lipopolysaccharide (LPS), a Toll-like receptor 4 agonist. EAY inhibited OVA- or LPS-induced $NF-{\kappa}B$ activation. EAY also suppressed OVA- or LPS-induced iNOS expression and nitrite production. These results suggest that EAY has the specific mechanism for anti-inflammatory responses and the potential to be developed as a potent anti-inflammatory and anti-allergic drug.

• The Korean Journal of Food And Nutrition
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• v.25 no.4
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• pp.863-870
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• 2012

Though hydrogen peroxide ($H_2O_2$) causes a deleterious effect to cells with its reactive oxygen species resulting in cell death, S-allyl cysteine (SAC, a bioactive organosulfur compound of aged garlic extract) has been known to have a cytoprotective effect. Few reported profiles of gene expression of $H_2O_2$ and SAC treated human cord blood derived mesenchymal stem cells (MSC). This study revealed changes in the profile of twenty-one genes grouped by oxidative stress, antioxidant, cell death, anti-apoptosis and anti-aging by quantitative real time PCR. A concentration of $100{\mu}M$ of SAC or $50{\mu}M$ of $H_2O_2$ was applied to MSC which show moderate growth and apoptosis pattern. $H_2O_2$ treatment enhanced expression of eleven genes out of twenty-one genes compared with that of control group, on the contrary SAC suppressed expression of eighteen genes out of twenty-one genes except C ros oncogene. SAC decreased expression of oxidative stress genes such as SOD1, CAT and GPX. These results seemed consistent with reports which elucidated over-expression of NF-${\kappa}$B by $H_2O_2$, and suppression of it by SAC. This study will confer basic information for further experiments regarding the effects of SAC on gene levels.

• Biomolecules & Therapeutics
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• v.24 no.4
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• pp.380-386
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• 2016

Silymarin from milk thistle (Silybum marianum) has been reported to show an anti-cancer activity. In previous study, we reported that silymarin induces cyclin D1 proteasomal degradation through NF-${\kappa}B$-mediated threonine-286 phosphorylation. However, mechanism for the inhibition of Wnt signaling by silymarin still remains unanswered. Thus, we investigated whether silymarin affects Wnt signaling in human colorectal cancer cells to elucidate the additional anti-cancer mechanism of silymarin. Transient transfection with a TOP and FOP FLASH luciferase construct indicated that silymarin suppressed the transcriptional activity of ${\beta}$-catenin/TCF. Silymarin treatment resulted in a decrease of intracellular ${\beta}$-catenin protein but not mRNA. The inhibition of proteasome by MG132 and $GSK3{\beta}$ inhibition by SB216763 blocked silymarin-mediated downregulation of ${\beta}$-catenin. In addition, silymarin increased phosphorylation of ${\beta}$-catenin and a point mutation of S33Y attenuated silymarin-mediated ${\beta}$-catenin downregulation. In addition, silymarin decreased TCF4 and increased Axin expression in both protein and mRNA level. From these results, we suggest that silymarin-mediated downregulation of ${\beta}$-catenin and TCF4 may result in the inhibition of Wnt signaling in human colorectal cancer cells.

• 한국약용작물학회:학술대회논문집
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• 2011.09a
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• pp.238-239
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• 2011

• BMB Reports
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• v.50 no.2
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• pp.85-90
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• 2017

Recently, we demonstrated that superoxide dismutase 3 (SOD3) is a strong candidate for biomedicine. Anti-oxidant function of SOD3 was accomplished without cell penetration, and it inhibited the inflammatory responses via non-enzymatic functions. SOD3 has the heparin binding domain associating cell surface. Interestingly, we found that $Zn^{2+}$ promotes transduction effects of recombinant human SOD3 (rhSOD3) by increasing uptake via the heparin binding domain (HBD). We demonstrated an uptake of rhSOD3 from media to cell lysate via HBD, resulting in an accumulation of rhSOD3 in the nucleus, which was promoted by the presence of $Zn^{2+}$. This resulted in increased inhibitory effects of rhSOD3 on NF-{\kappa}B and STAT3 signals in the presence of $Zn^{2+}$, which shows elevated association of rhSOD3 into the cells. These results suggest that an optimized procedure can help to enhance the inflammatory efficacy of rhSOD3, as a novel biomedicine.

• Fisheries and Aquatic Sciences
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• v.12 no.2
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• pp.90-97
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• 2009

The cytoskeletal $\beta$-actin gene and its 5'-upstream region were isolated and characterized in the rockbream (Oplegnathus fasciatus). Complementary DNA of the rockbream $\beta$-actin represented a 1,125 bp of an open reading frame encoding 375 amino acids, and the rockbream $\beta$-actin cDNA and deduced amino acid sequences were highly homologous to those of other vertebrate orthologs. At the genomic level, the $\beta$-actin gene also exhibited an organization typical of vertebrate cytoskeletal actin genes (2,159 bp composed of five translated exons interrupted by four introns) with a conserved GT/AG exon-intron splicing rule. The putative non-translated exon predicted in the rockbream $\beta$-actin gene was much more homologous with those of teleostean $\beta$-actin genes than those of mammals. The 5'-upstream regulatory region isolated by genome walking displayed conserved and essential elements such as TATA, CArG and CAAT boxes in its proximal part, while several other immune- or stress-related motifs such as those for NF-kappa B, USF, HNF, AP-1 and C/EBP were in the distal part. Semi-quantitative RT-PCR assay results demonstrated that the rockbream $\beta$-actin transcripts were ubiquitously but different-tially expressed across the tissues of juveniles.

• Nutrition Research and Practice
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• v.9 no.2
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• pp.117-122
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• 2015

BACKGROUND/OBJECTIVES: Curcumin, a major component of the Curcuma species, contains antioxidant and anti-inflammatory properties. Although it was found to induce apoptosis in cancer cells, the functional role of curcumin as well as its molecular mechanism in anti-inflammatory response, particularly in intestinal cells, has been less investigated. The intestine epithelial barrier is the first barrier and the most important location for the substrate coming from the lumen of the gut. SUBJECTS/METHODS: We administered curcumin treatment in the human intestinal epithelial cell lines, T84 and Caco-2. We examined endoplasmic reticulum (ER) stress response by thapsigargin, qPCR of XBP1 and BiP, electrophysiology by wild-type cholera toxin in the cells. RESULTS: In this study, we showed that curcumin treatment reduces ER stress and thereby decreases inflammatory response in human intestinal epithelial cells. In addition, curcumin confers protection without damaging the membrane tight junction or actin skeleton change in intestine epithelial cells. Therefore, curcumin treatment protects the gut from bacterial invasion via reduction of ER stress and anti-inflammatory response in intestinal epithelial cells. CONCLUSIONS: Taken together, our data demonstrate the important role of curcumin in protecting the intestine by modulating ER stress and inflammatory response post intoxication.