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首页> 外文期刊>Cellular Physiology and Biochemistry >(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice
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(-)-Epigallocatechin-3-Gallate Inhibits Arsenic-Induced Inflammation and Apoptosis through Suppression of Oxidative Stress in Mice

机译:(-)-Epigallocatechin-3-Gallate通过抑制小鼠的氧化应激抑制砷诱导的炎症和细胞凋亡

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>Background/Aims: Exposure to arsenic in individuals has been found to be associated with various health-related problems including skin lesions, cancer, and cardiovascular and immunological disorders. (-)-Epigallocatechin-3-gallate (EGCG), the main and active polyphenolic catechin present in green tea, has shown potent antioxidant, anti-apoptotic and anti-inflammatory activity in vivo and in vitro. Thus, the present study was conducted to investigate the protective effects of EGCG against arsenic-induced inflammation and immunotoxicity in mice. Methods: Serum IL-1?2, IL-6 and TNF-?± were determined by ELISA, tissue catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), nitric oxide and caspase 3 by commercial kits, mitochondrial membrane potential with Rh 123, mitochondrial ROS with 2a€?,7a€?-dichlorofluorescin diacetate (DCFH-DA), apoptotic and necrotic cells and T-cell phenotyping with Flow cytometry analysis. Results: The results showed that arsenic treatment significantly increased oxidative stress levels (as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione and reactive oxygen species), increased levels of inflammatory cytokines and promoted apoptosis. Arsenic exposure increased the relative frequency of the CD8+(Tc) cell subpopulation (from 2.8 to 18.9%) and decreased the frequency of CD4+(Th) cells (from 5.2 to 2.7%). Arsenic exposure also significantly decreased the frequency of T(CD3) (from 32.5% to 19.2%) and B(CD19) cells (from 55.1 to 32.5%). All of these effects induced by NaAsO2 were attenuated by EGCG. Conclusions: The present in vitro findings indicate that EGCG attenuates not only NaAsO2-induced immunosuppression but also inflammation and apoptosis.
机译:> 背景/目标: 人们发现接触砷与多种健康相关的问题有关,包括皮肤损害,癌症以及心血管和免疫疾病。 (-)-表没食子儿茶素-3-没食子酸酯(EGCG)是绿茶中存在的主要和活性多酚儿茶素,在体内 和已显示出有效的抗氧化剂,抗凋亡和抗炎活性体外。因此,进行本研究以研究EGCG对砷诱导的小鼠炎症和免疫毒性的保护作用。 方法: 用ELISA,组织过氧化氢酶(CAT),丙二醛(MDA),超氧化物歧化酶( SOD),谷胱甘肽(GSH),一氧化氮和胱天蛋白酶3(通过商业试剂盒提供),线粒体膜电位与Rh 123,线粒体ROS与2a?,7a?-二氯二氟二乙酸双乙酸酯(DCFH-DA),凋亡和坏死细胞以及T-流式细胞仪分析细胞表型 结果: 结果表明,砷处理显着增加了氧化应激水平(如过氧化氢酶,丙二酰二醛,超氧化物歧化酶,谷胱甘肽和活性氧种类),增加了炎性细胞因子的水平并促进细胞凋亡砷暴露增加了CD8 +(Tc)细胞亚群的相对频率(从2.8到18.9%),并降低了CD4 +(Th)细胞的频率(从5.2到2.7%)。砷暴露还显着降低了T(CD3)细胞(从32.5%降低到19.2%)和B(CD19)细胞(从55.1降低到32.5%)的频率。 NaAsO 2 诱导的所有这些作用均被EGCG减弱。 结论: 目前的体外发现表明EGCG不仅减弱了NaAsO 2 诱导的免疫抑制作用,而且还减弱了炎症和细胞凋亡。

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