[钙抑制剂对培养的牛主动脉内皮细胞中过氧化氢诱导的损伤及钙内流的影响]

[Effects of calcium inhibitor on hydrogen peroxide-induced damage and calcium influx in bovine aortic endothelial cells in culture].

作者信息

Tao X B, Li W H, Huang M, Tan Y X, Yuan M, Zhou B

机构信息

Research Laboratory of Natural and Synthetic Drugs, College of Pharmacy, Second Military Medical University, Shanghai 200433.

出版信息

Yao Xue Xue Bao. 1997 Jul;32(7):485-9.

PMID:11596271

Abstract

Hydrogen peroxide(H2O2)-induced cell damage and Ca2+ influx into bovine aortic endothelial cells (BAEC) were investigated. Our data suggested that H2O2 could dose- and time-dependently induce damage in cultured BAEC assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT) assay and increase malondialdehyde (MDA) production, which reflects the level of lipid peroxidation. Exposure of BAEC to H2O2 (100 mumol.L-1) caused significant increase in intracellular free calcium ([Ca2+]i) within 6 min, suggesting that the increase of [Ca2+]i might implicate in H2O2-induced cell damage. The calcium inhibitor nifedipine was found to dose-dependently decrease the increase of [Ca2+]i caused by H2O2 and protect BAEC against H2O2-induced damage reflected by significant decrease of MDA production and increase of MTT value. These results indicate that overload of calcium might be responsible to some extent causing oxidative damage to cells.

摘要

研究了过氧化氢（H2O2）诱导的细胞损伤以及Ca2+流入牛主动脉内皮细胞（BAEC）的情况。我们的数据表明，H2O2可通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴盐（MTT）试验剂量和时间依赖性地诱导培养的BAEC损伤，并增加丙二醛（MDA）的产生，MDA的产生反映了脂质过氧化水平。将BAEC暴露于H2O2（100μmol·L-1）在6分钟内导致细胞内游离钙（[Ca2+]i）显著增加，表明[Ca2+]i的增加可能与H2O2诱导的细胞损伤有关。发现钙抑制剂硝苯地平可剂量依赖性地减少H2O2引起的[Ca2+]i增加，并保护BAEC免受H2O2诱导的损伤，这表现为MDA产生显著减少和MTT值增加。这些结果表明，钙超载可能在一定程度上导致细胞氧化损伤。