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首页> 外文期刊>Cell Research >Parthenolide protects human lens epithelial cells from oxidative stress-induced apoptosis via inhibition of activation of caspase-3 and caspase-9
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Parthenolide protects human lens epithelial cells from oxidative stress-induced apoptosis via inhibition of activation of caspase-3 and caspase-9

机译：偏苯二酚通过抑制caspase-3和caspase-9的活化来保护人晶状体上皮细胞免受氧化应激诱导的细胞凋亡

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The apoptosis of lens epithelial cells has been proposed as the common basis of cataract formation, with oxidative stress as the major cause. This study was performed to investigate the protective effect of the herbal constituent parthenolide against oxidative stress-induced apoptosis of human lens epithelial (HLE) cells and the possible molecular mechanisms involved. HLE cells (SRA01-04) were incubated with 50 μM H_2O_2 in the absence or presence of different doses of parthenolide (10, 20 and 50 μM). To study apoptosis, the cells were assessed by morphologic examination and Annexin V-propidium iodide double staining flow cytometry; to investigate the underlying molecular mechanisms, the expression of caspase-3 and caspase-9 were assayed by Western blot and quantitative RT-PCR, and the activities of caspase-3 and caspase-9 were measured by a Chemicon caspase colorimetric activity assay kit. Stimulated with H_2O_2 for 18 h, a high fraction of HLE cells underwent apoptosis, while in the presence of parthenolide of different concentrations, dose-dependent blocking of HLE cell apoptosis was observed. The expression of caspase-3 and caspase-9 induced by H_2O_2 in HLE cells was significantly reduced by parthenolide both at the protein and mRNA levels, and the activation of caspase-3 and caspase-9 was also suppressed by parthenolide in a dose-dependent manner. In conclusion, parthenolide prevents HLE cells from oxidative stress-induced apoptosis through inhibition of the activation of caspase-3 and caspase-9, suggesting a potential protective effect against cataract formation.
机译：已经提出晶状体上皮细胞的凋亡是白内障形成的常见基础，氧化应激是主要原因。进行这项研究的目的是研究中草药组成的单身粉酚对氧化应激诱导的人晶状体上皮细胞（HLE）细胞凋亡的保护作用及其可能的分子机制。在不存在或存在不同剂量的小白菊内酯（10、20和50μM）的情况下，将HLE细胞（SRA01-04）与50μMH_2O_2孵育。为了研究细胞凋亡，通过形态学检查和膜联蛋白V-碘化丙啶双染色流式细胞术评估细胞；为了研究潜在的分子机制，通过蛋白质印迹和定量RT-PCR检测caspase-3和caspase-9的表达，并使用Chemicon caspase比色活性检测试剂盒测量caspase-3和caspase-9的活性。 H_2O_2刺激18 h，高比例的HLE细胞发生凋亡，而在不同浓度的小白菊内酯存在下，剂量依赖性阻断HLE细胞凋亡。单酚内酯在蛋白和mRNA水平上均可显着降低H_2O_2诱导HLE细胞caspase-3和caspase-9的表达，且剂量依赖性的单酚抑制caspase-3和caspase-9的活化。方式。总之，小白菊内酯通过抑制caspase-3和caspase-9的活化来防止HLE细胞氧化应激诱导的细胞凋亡，提示其对白内障形成的潜在保护作用。

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