目的 探讨依达拉奉(EDA)对氧化应激诱导的肺泡Ⅱ型上皮细胞凋亡的影响及可能机制.方法 用过氧化氢氧化应激建立氧化应激肺泡Ⅱ型上皮细胞凋亡模型细胞.将细胞分为:过氧化氢处理组(H组)、依达拉奉-过氧化氢处理组(E组)和对照组(C组).采用脂质过氧化物(MDA)、谷胱甘肽(GSH)试剂盒检测A549细胞MDA、GSH的含量,同时测定三组细胞生长的抑制率、凋亡率、半胱氨酸天冬氨酸蛋白酶(caspase)-3与caspase-9 mRNA及蛋白表达.结果 与C组比较,H组细胞MDA、细胞生长抑制率、凋亡指数、caspase-3与caspase-9 mRNA相对表达及蛋白表达量明显升高;而GSH明显降低(P<0.01).与H组比较,E组细胞MDA、细胞生长抑制率、凋亡指数、caspase-3与caspase-9 mRNA相对表达及蛋白表达量明显降低;而GSH明显增高(P<0.05).结论 依达拉奉可通过抗氧化及抗caspase-3,caspase-9引起的凋亡以保护肺泡Ⅱ型上皮细胞对抗氧化应激.%Objective Our present study was undertaken to explore the effects of edaravone on lung epithelial type Ⅱ cells against apoptosis induced by oxidative stress. Methods Lung epithelial Type Ⅱ cells with H2O2 treatment were divided into three groups: hydrogen peroxide group (group Ⅲ), edaravone-treated hydrogen peroxide group (group E) and control group (group C). Malonic dialed hyde (MDA), glutathione (GSH), cell inhibition ration, apoptosis rate, caspase-3, and caspase-9 were determined in each group. Results Compared with group C, cell inhibition ration was significantly increased accompanied by elevated MDA content, apoptosis rate, caspase-3, and caspase-9 Mrna and protein expression in group Ⅲ, while the content of GSH were reduced (P<0. 01). Compared with group Ⅲ,the MDA, cell inhibition, apoptosis rate, caspase-3 and caspase-9 Mrna and protein were decreased while GSH were increased in group E(P<0. 05). Conclusion Edaravone can reduce apoptosis of lung epithelial Type Ⅱ cells induced by oxidative stress, which might be due to the inhibition of caspase-3 and caspase-9 expressioa
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