Publications (469) View all
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Article: SoSoSo or its active ingredient chrysophanol regulates production of inflammatory cytokines & adipokine in both macrophages & adipocytes.
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ABSTRACT: Background & objectives: Obesity is now considered as a major risk factor for the development of fatty liver diseases, cardiovascular diseases, and atherosclerosis. SoSoSo is a newly developed dietary supplement made of seven medicinal herbs. This study was aimed at examining the anti-obesity effect of SoSoSo or its active ingredient chrysophanol on the production of inflammatory cytokines and adipokine in macrophyage cell line RAW264 and 3T3-L1 adipocytes. Methods: No release was measured as a form of nitrite by Griess method. The production of inflammatory cytokines and adipokine were measured with the ELISA method. The m-RNA expression of each cytokine and adipokine were measured using RT-PCR. The nuclear proteins for NF-κB were analyzed with western blotting. Results: SoSoSo or chrysophanol significantly inhibited the nitric oxide production in lipopolysaccharide-stimulated RAW264 cells as well as in RAW264 cells-conditioned medium (CM)-treated 3T3-L1 cells. The production of interleukin (IL)-6 and tumour necrosis factor (TNF)-α were inhibited by SoSoSo or chrysophanol. In addition, SoSoSo or chrysophanol inhibited the activation of nuclear factor-κB in RAW264 cells. SoSoSo or chrysophanol inhibited the productions of IL-6, TNF-α, and monocyte chemoattractant protein-1 as well as the reduction of adiponectin production in CM-treated 3T3-L1 cells. Interpretation & conclusions: These results suggest a potential of SoSoSo or chrysophanol as a source of anti-inflammatory agent for obesity. Further in vivo studies would be required to confirm these findings.The Indian journal of medical research 01/2013; 137(1):142-150. · 1.84 Impact Factor -
Article: Candidate genes of cerebrovascular disease and sudden sensorineural hearing loss.
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ABSTRACT: Auditory dysfunction is related to large/small vessel occlusions and hemorrhage. Sudden sensorineural hearing loss (SSNHL) frequently occurs with anterior inferior cerebellar artery occlusion proximal to the internal auditory artery. Moreover, SSNHL has various pathogenetic mechanisms, the main proposed mechanisms being vascular disease, membrane ruptures, infection, and autoimmunity. Tumor necrosis factor (TNF) is an important cytokine in the inflammation process of cerebrovascular diseases. In the current study, the possible effects of polymorphisms in TNF-alpha and TNF-beta genes on SSNHL are evaluated. Two genetic polymorphisms in the TNF locus (TNF-alpha -308 G - ->A and TNF-beta +252 A - ->G) were investigated as risk factors for SSNHL by determining their prevalence in 97 SSNHL patients and in 587 controls. A significant increase was found for the TNF-beta allele 1 in SSNHL patients compared with the controls (chi( 2) = 7.251, P = .007, odds ratio [OR] = 1.534, confidence interval [CI] = 1.12-2.10). These findings suggest that the TNF-beta +252 locus plays an important role in the etiopathogenesis of SSNHL.Clinical and Applied Thrombosis/Hemostasis 10/2009; 16(5):559-62. · 1.33 Impact Factor -
Article: Anti-inflammatory effect of Columbianetin on activated human mast cells.
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ABSTRACT: In the present study, we extracted Corydalis heterocarpa with various solvents in order to find the bioactive constituents that demonstrated anti-inflammatory effects. We isolated the active compound, Columbianetin. Anti-inflammatory effect of Columbianetin has been reported but the precise effects of Columbianetin in experimental models have remained unknown. In the present study, we investigate the effect of Columbianetin on the production of histamine, interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor (TNF)-alpha and expression of cyclooxygenase-2 (COX-2) by using the human mast cell line (HMC-1). Various concentrations of Columbianetin were treated before the activation of HMC-1 cells with phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore, A23187. PMA plus A23187 significantly increased IL-1beta, IL-6, IL-8, and TNF-alpha production compared with media control (p<0.05). We also show that the increased cytokines IL-1beta, IL-6, IL-8, and TNF-alpha level was significantly inhibited by Columbianetin in a dose-dependent manner (p<0.05). Maximal inhibition rates of IL-1beta, IL-6, IL-8, and TNF-alpha production by Columbianetin were about 102.6%, 101.1%, 95.8%, and 103.9%, respectively. Columbianetin inhibited expression of COX-2. In addition, the effect of Columbianetin was investigated on the histamine release from HMC-1 stimulated by substance P, which promotes histamine release. Columbianetin also inhibited the histamine release by substance P. In conclusion, these results indicate that Columbianetin may be helpful in regulating mast cell-mediated allergic inflammatory responses.Biological & Pharmaceutical Bulletin 06/2009; 32(6):1027-31. · 1.66 Impact Factor -
Article: Expression of inducible nitric oxide synthase by Corydalis turtschaninovii on interferon-gamma stimulated macrophages.
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ABSTRACT: Corydalis turtschaninovii (CT) has been used for tumor therapy. However, it is still unclear how this herb prevents the diseases in experimental models. Nitric oxide (NO) as a potent macrophage-derived effector molecule against a variety of tumors has received increasing attention. In this study, using mouse peritoneal macrophages, we have examined the mechanism by which CT regulates NO production. When CT was used in combination with recombinant interferon-gamma (rIFN-gamma), there was a marked cooperative induction of NO production. However, CT had no effect on NO production by itself. The increase in NO synthesis was reflected as an increased amount of inducible NO synthase (iNOS) protein. The increased production of NO from rIFN-gamma plus CT-stimulated peritoneal macrophages was decreased by the treatment with N(G)-monomethyl-L-arginine or N(alpha)-Tosyl-Phe Chloromethyl Ketone, iNOS inhibitor. The increased production of NO from rIFN-gamma plus CT-stimulated cells was almost completely inhibited by pre-treatment with pyrrolidine dithiocarbamate, an inhibitor of nuclear factor kappa B (NF-kappaB). However, treatment of peritoneal macrophages with rIFN-gamma plus CT had no effect on the increase in tumor necrosis factor-alpha (TNF-alpha) production. Our findings demonstrate that CT increases the production of NO and TNF-alpha by rIFN-gamma-primed macrophages and suggest that NF-kappaB plays a critical role in mediating these effects of CT.Journal of ethnopharmacology 05/2009; 122(3):573-8. · 2.32 Impact Factor -
Article: A novel histone deacetylase (HDAC) inhibitor MHY219 induces apoptosis via up-regulation of androgen receptor expression in human prostate cancer cells.
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ABSTRACT: Histone deacetylase (HDAC) inhibitors are a new class of anticancer agents that act by inhibiting cancer cell proliferation and inducing apoptosis in various cancer cell lines. To investigate the anticancer effect of a novel histone deacetylase (HDAC) inhibitor MHY219, its efficacy was compared to that of suberoylanilide hydroxamic acid (SAHA) in human prostate cancer cells. The anticancer effects of MHY219 on cell viability, HDAC enzyme activity, cell cycle regulation, apoptosis and other biological assays were performed. MHY219 was shown to enhance the cytotoxicity on DU145 cells (IC50, 0.36μM) when compared with LNCaP (IC50, 0.97μM) and PC3 cells (IC50, 5.12μM). MHY219 showed a potent inhibition of total HDAC activity when compared with SAHA. MHY219 increased histone H3 hyperacetylation and reduced the expression of class I HDACs (1, 2 and 3) in prostate cancer cells. MHY219 effectively increased the sub-G1 fraction of cells through p21 and p27 dependent pathways in DU145 cells. MHY219 significantly induced a G2/M phase arrest in DU145 and PC3 cells and arrested the cell cycle at G0/G1 phase in LNCaP cells. Furthermore, MHY219 effectively increased apoptosis in DU145 and LNCaP cells, but not PC3 cells, according to Annexin V/PI staining and Western blot analysis. These results indicate that MHY219 is a potent HDAC inhibitor that targets regulating multiple aspects of cancer cell death and might have preclinical value in human prostate cancer chemotherapy, warranting further investigation.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 02/2013; · 2.24 Impact Factor
