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Inhibition of nuclear factor-kappa B activation attenuates hydrogen peroxide-induced cytotoxicity in human lens epithelial cells

机译:抑制核因子-κB激活减弱人晶状体上皮细胞中过氧化氢诱导的细胞毒性

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摘要

Aims: Hydrogen peroxide (H2O2) is the major oxidant involved in cataract formation. Lens epithelial cells have been suggested to be the first site of oxidative damage. The authors investigated the relationship between H2O2-induced cytotoxicity and activation of nuclear factor kappa B (NF-B) in human lens epithelial (HLE) cells. Methods: HLE B-3 cells were stimulated by various concentrations of H2O2 in the presence or absence of pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of NF-B. H2O2-induced cytotoxicity was measured by lactate dehydrogenase cytotoxicity assay. Translocation of NF-B was examined by Western blot and immunocytochemistry using anti-p65 antibody. Results: H2O2-induced cytotoxicity increased in a concentration-dependent manner. PDTC treatment significantly suppressed the cytotoxicity induced by H2O2. After stimulated with H2O2, NF-B was found translocated from cytoplasm into the nuclei. PDTC treatment also inhibited the translocation of NF-B. Conclusions: NF-B signal pathway may be important in the development of H2O2-induced damage in HLE cells that is involved in cataractogenesis.
机译:目的:过氧化氢(H2O2)是参与白内障形成的主要氧化剂。晶状体上皮细胞被认为是氧化损伤的第一个部位。作者研究了H2O2诱导的细胞毒性与人晶状体上皮细胞(HLE)中核因子κB(NF-B)活化之间的关系。方法:在存在或不存在吡咯烷二硫代氨基甲酸酯(PDTC)(一种有效的NF-B抑制剂)下,用各种浓度的H2O2刺激HLE B-3细胞。 H2O2诱导的细胞毒性通过乳酸脱氢酶细胞毒性测定来测量。通过Western印迹和使用抗p65抗体的免疫细胞化学检查了NF-B的易位。结果:H2O2诱导的细胞毒性以浓度依赖性方式增加。 PDTC处理显着抑制了H2O2诱导的细胞毒性。用H2O2刺激后,发现NF-B从细胞质转移到细胞核中。 PDTC处理也抑制了NF-B的转运。结论:NF-B信号通路可能在H2O2诱导的HLE细胞损伤中的发展中起重要作用,该损伤与白内障的发生有关。

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