MnTMPyP通过抑制线粒体凋亡通路对百草枯诱导肺上皮细胞损伤的保护作用

doi:10.3969/j.issn.1002-1949.2018.10.014

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摘要目的探讨MnTMPyP(Mn)通过抑制氧化应激和线粒体凋亡通路对百草枯(PQ)诱导肺上皮细胞损伤的保护作用。方法体外培养人肺泡Ⅱ型上皮样细胞A549细胞，以超氧化物歧化酶(SOD)的模拟物Mn为干预因素。实验分为四组：①对照组：加入RPMI 1640培养液；②Mn组：加入Mn 10 μmol/L； ③PQ组：加入PQ 750 μmol/L；④PQ+Mn组：Mn 10 μmol/L预处理90 min，再加入PQ 750 μmol/L。各组细胞处理24 h后检测相关指标。MTT法检测细胞活性；流式细胞术检测细胞凋亡率、线粒体膜电位、活性氧（ROS）；分光光度法检测Caspase-3；Western blotting检测线粒体凋亡蛋白Bcl-2、Bax蛋白的表达。结果与对照组比较，Mn组检测指标无统计学意义；PQ组细胞活性降低，细胞凋亡率增加有统计学意义（P<0.01），线粒体膜电位降低有统计学意义（P<0.01），ROS的产生显著增加， Caspase-3活性增高，Western blotting显示线粒体凋亡途径中抗凋亡蛋白Bcl-2表达量降低，促凋亡蛋白Bax表达增强。与PQ组比较，PQ+Mn组细胞活性增加，细胞凋亡率降低，线粒体膜电位增强，ROS的产生减少，Caspase-3活性降低，Western blotting显示Bcl-2蛋白表达量增强，Bax蛋白表达降低。结论 Mn有效减轻PQ诱导肺上皮细胞的损伤，其机制是和拮抗PQ引起的氧化应激诱导的线粒体凋亡途径有关。

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	许勇民
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	董雪松

关键词 ： MnTMPyP, 百草枯(PQ), 肺上皮细胞, 氧化应激, 凋亡

基金资助:国家自然科学基金（81471851）；辽宁省博士启动基金（20141033）

通讯作者: 董雪松(1978-)，男，博士，副教授，副主任医师，E-mail:dongxues@163.com。

作者简介: 许勇民（1987-），男，硕士研究生。

引用本文:

许勇民，宋春青，孙大壮，王蕊，董雪松. MnTMPyP通过抑制线粒体凋亡通路对百草枯诱导肺上皮细胞损伤的保护作用[J]. 中国急救医学, 2018, 38(10): 900-905.
Xu Yong-min, Song Chun-qing, Sun Da-zhuang, Wang Rui, Dong Xue-song. MnTMPyP protects paraquat-induced lung epithelial-like cell injury through inhibition of oxidative stress and mitochondrial apoptosis pathway. Chinese Journal of Critical Care Medicine, 2018, 38(10): 900-905.

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http://www.cnemergency.org.cn/CN/10.3969/j.issn.1002-1949.2018.10.014 或 http://www.cnemergency.org.cn/CN/Y2018/V38/I10/900

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