Objective The aim of this study is to evaluate the cytoprotection and potential molecular mechanisms of cyanidin-3-glucoside (C3G) on hydrogen peroxide (H 2 O 2 )-induced oxidative damage in HepG2 cells. Methods The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was carried out to examine the viability of HepG2 cells exposure to H 2 O 2 or C3G. Meanwhile, the antioxidant properties of C3G were measured by determining the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and the malondialdehyde (MDA) levels. Flow cytometry was employed to determine HepG2 cells apoptosis, and HepG2 cells were stained with Hoechst 33342 to observe cell morphology. 2′,7′-dichlorofluorescin diacetate (DCFH-DA) was used to evaluate the production of intracellular reactive oxygen species (ROS). Finally, the expression of apoptosis-related protein was monitored through western blot analysis. Results HepG2 cells induced with H 2 O 2 presented a remarkable decrease in cell viability that was suppressed when HepG2 cells were interfered with C3G (2.5–10 μM). C3G interference memorably and dose-dependently inhibited H 2 O 2 -induced intracellular ROS and MDA overproduction, while C3G treatment markedly increased H 2 O 2 -induced the activities of intracellular SOD, GSH-Px and CAT. Eventually, the relative proteins expression levels of p53, cleaved caspase-9/3, cytochrome c, Fas-L, Fas, FADD and caspase-8 were substantially up-regulated in H 2 O 2 -triggered HepG2 cells, and Bax/Bcl-2 ratio and the relative protein expression levels of PARP were dramatically down-regulated. However, the expression levels of these relative proteins were reversed in C3G-interfered HepG2 cells. Conclusions C3G could protect HepG2 cells from oxidative damage, and the effects that were mediated by the mitochondrial apoptotic pathways and the external pathways.

中文翻译：

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Cyanidin-3-glucoside 防止过氧化氢 (H2O2) 诱导的 HepG2 细胞氧化损伤

目的 本研究的目的是评估 cyanidin-3-glucoside (C3G) 对过氧化氢 (H 2 O 2 ) 诱导的 HepG2 细胞氧化损伤的细胞保护作用和潜在分子机制。方法 进行3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑(MTT) 测定以检测HepG2 细胞暴露于H 2 O 2 或C3G 的活力。同时，通过测定超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）和丙二醛（MDA）水平的活性来测量C3G的抗氧化性能。流式细胞术检测HepG2细胞凋亡，Hoechst 33342染色HepG2细胞，观察细胞形态。2',7'-二氯荧光素二乙酸酯 (DCFH-DA) 用于评估细胞内活性氧 (ROS) 的产生。最后，通过蛋白质印迹分析监测细胞凋亡相关蛋白的表达。结果 H 2 O 2 诱导的 HepG2 细胞呈现出细胞活力的显着降低，当 HepG2 细胞受到 C3G (2.5–10 μM) 干扰时，这种降低会受到抑制。C3G 干扰显着地且剂量依赖性地抑制了 H 2 O 2 诱导的细胞内 ROS 和 MDA 过量产生，而 C3G 处理显着增加了 H 2 O 2 诱导的细胞内 SOD、GSH-Px 和 CAT 的活性。最终，在 H 2 O 2 触发的 HepG2 细胞和 Bax/Bcl 中，p53、裂解的 caspase-9/3、细胞色素 c、Fas-L、Fas、FADD 和 caspase-8 的相对蛋白表达水平显着上调-2 比率和 PARP 的相对蛋白质表达水平显着下调。然而，这些相关蛋白的表达水平在 C3G 干扰的 HepG2 细胞中被逆转。结论 C3G 可以保护 HepG2 细胞免受氧化损伤，以及由线粒体凋亡途径和外部途径介导的作用。