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作 者:陈子盛[1] 傅应云[1] 刘盛国[1] 何正强[1]
机构地区:[1]暨南大学第二临床医学院深圳市人民医院呼吸科,广东深圳518020
出 处:《中国药理学通报》2013年第1期132-135,共4页Chinese Pharmacological Bulletin
摘 要:目的观察白介素-15(IL-15)对H2O2诱导的大鼠Ⅱ型肺泡上皮细胞凋亡的影响及探讨其机制。方法体外培养大鼠Ⅱ型肺泡上皮细胞(RLE-6TN),分为:(A)正常对照组;(B)IL-15预处理组;(C)H2O2损伤组;(D)IL-15预处理后H2O2损伤组。采用DAPI荧光染色及Annexin V-FITC/PI检测各组细胞凋亡,JC-1染色观察各组线粒体膜电位;RT-PCR检测各组细胞Bcl-2、Bax、Caspase-3 mRNA表达。结果与正常对照组比较,H2O2损伤能明显诱导RLE-6TN凋亡,IL-15预处理可明显降低H2O2诱导的细胞凋亡率,使细胞线粒体膜电位下降,Bcl-2 mRNA表达增加,Bax、Caspase-3mRNA表达降低(P<0.05)。结论 IL-15能抑制H2O2诱导的大鼠Ⅱ型肺泡上皮细胞凋亡,其作用机制可能为稳定细胞线粒体膜电位,增强抗凋亡基因Bcl-2,同时,抑制促凋亡基因Bax表达,下调Caspase-3表达。Aim To study the effect of interleukin-15 (IL-15) on the rat type Ⅱalveolar epithelial cells (RLE-6TN) apoptosis induced by hydrogen peroxide (H202 ). Methods The experimental RLE-6TN were cultured in vivo, which were divided into four groups: (A) normal control group; (B) pre-treated group with IL-15; (C) injured group with H202; (D)the group pre-treated with IL-15 and injured successively by H202. Cell apoptosis was detected by DAPI staining and Annexin V-FITC/PI; the change of mitochondrial membrane potential was observed by JC-1 staining; the expression of Bcl-2, Bax and Caspase-3 mRNA of RLE-6TN were detected by RT-PCR. Results Com-pared with the control group, H202 induced cells apop- tosis obviously (P 〈 0.05). But IL-15 significantly re- duced the rate of H202-induced cell apoptosis, mito- chondrial membrane potential and expression of Bax and Caspase-3 mRNA. While it significantly increased the expression of Bcl-2 mRNA. Conclusion IL-15 inhibits the H2 02 -induced apoptosis of type Ⅱ alveolar epithelial cells. It may protect the mitochondrial mem- brane potential, and promot the gene expression of Bcl- 2, inhibit the Bax and Caspase-3 expression.
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