Jin Xue-Hai, Ohgami Kazuhiro, Shiratori Kenji, Koyama Yoshikazu, Yoshida Kazuhiko, Kase Satoru, Ohno Shigeaki
Department of Ophthalmology and Visual Sciences, Hokkaido University Graduate School of Medicine, North 15, West 7, Kita-ku, Sapporo 060-8638, Japan.
Br J Ophthalmol. 2007 Mar;91(3):369-71. doi: 10.1136/bjo.2006.107037. Epub 2006 Oct 4.
Hydrogen peroxide (H(2)O(2)) 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 H(2)O(2)-induced cytotoxicity and activation of nuclear factor kappa B (NF-kappaB) in human lens epithelial (HLE) cells.
HLE B-3 cells were stimulated by various concentrations of H(2)O(2) in the presence or absence of pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of NF-kappaB. H(2)O(2)-induced cytotoxicity was measured by lactate dehydrogenase cytotoxicity assay. Translocation of NF-kappaB was examined by Western blot and immunocytochemistry using anti-p65 antibody.
H(2)O(2)-induced cytotoxicity increased in a concentration-dependent manner. PDTC treatment significantly suppressed the cytotoxicity induced by H(2)O(2). After stimulated with H(2)O(2), NF-kappaB was found translocated from cytoplasm into the nuclei. PDTC treatment also inhibited the translocation of NF-kappaB.
NF-kappaB signal pathway may be important in the development of H(2)O(2)-induced damage in HLE cells that is involved in cataractogenesis.
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起始部位。作者研究了H₂O₂诱导的细胞毒性与人类晶状体上皮（HLE）细胞中核因子κB（NF-κB）激活之间的关系。
在存在或不存在吡咯烷二硫代氨基甲酸盐（PDTC，一种有效的NF-κB抑制剂）的情况下，用不同浓度的H₂O₂刺激HLE B-3细胞。通过乳酸脱氢酶细胞毒性测定法测量H₂O₂诱导的细胞毒性。使用抗p65抗体通过蛋白质印迹和免疫细胞化学检测NF-κB的易位。
H₂O₂诱导的细胞毒性呈浓度依赖性增加。PDTC处理显著抑制了H₂O₂诱导的细胞毒性。用H₂O₂刺激后，发现NF-κB从细胞质转移到细胞核。PDTC处理也抑制了NF-κB的易位。
NF-κB信号通路在参与白内障发生的HLE细胞中H₂O₂诱导的损伤发展过程中可能很重要。
