Irisin对H9C2心肌细胞缺氧复氧损伤后的保护作用

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摘要目的观察鸢尾素（Irisin）对缺氧复氧处理后H9C2心肌细胞的保护作用。方法将大鼠H9C2心肌细胞分为对照组、对照+Irisin组、缺氧复氧组、缺氧复氧+Irisin组。对照组正常培养，对照+Irisin组正常培养并给予10 ng/mL的Irisin，缺氧复氧组细胞行缺氧复氧处理，缺氧复氧+Irisin组细胞进行缺氧复氧处理后再加入10 ng/mL的Irisin。通过CCK-8检测心肌细胞活力，活性氧（ROS）荧光探针检测细胞内ROS含量，流式细胞术检测线粒体膜电位JC-1。利用RT-PCR检测心肌细胞caspase-3和caspase-9的mRNA含量。结果缺氧复氧组细胞活力显著低于对照组（P ＜ 0.01）；缺氧复氧+Irisin组细胞活力高于缺氧复氧组（P ＜ 0.05）。缺氧复氧组细胞内ROS水平高于对照组（P ＜ 0.01）；缺氧复氧+Irisin组ROS水平低于缺氧复氧组（P ＜ 0.05）。缺氧复氧组线粒体膜电位JC-1水平低于对照组（P ＜ 0.05）；缺氧复氧+Irisin组线粒体膜电位JC-1水平高于缺氧复氧组（P ＜ 0.05）。缺氧复氧组caspase-3及caspase-9的mRNA水平高于对照组（P ＜ 0.05）；缺氧复氧+Irisin组caspase-3及caspase-9的mRNA水平低于缺氧复氧组（P ＜ 0.05）。结论 Irisin可提高心肌细胞缺氧复氧处理后的细胞活力，减少ROS生成，恢复线粒体膜电位，抑制凋亡通路，可作为改善心肌缺血再灌注损伤的潜在治疗药物。

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	吴娟1 张晓萌1 常盼1 朱肖星2 李静1 王西辉1 王建榜1 于军3

关键词 ：缺氧复氧, H9C2, 活性氧, 心肌损伤, 凋亡

Abstract：Objective To observe the protective effect of Irisin on H9C2 cardiomyocytes after hypoxia reoxygenation. Methods Rat H9C2 cardiomyocytes were divided into control group, control+Irisin group, hypoxia-reoxygenation group, hypoxia-reoxygenation+Irisin group. The control group was cultured normally. The control +Irisin group was cultured normally and given 10 ng/mL of Irisin. The hypoxia-reoxygenation group was treated with hypoxia-reoxygenation, and the cells of hypoxia-reoxygenation+Irisin group were treated with hypoxia-reoxygenation and 10 ng/mL of Irisin. Cell viability was detected by CCK-8. Reactive exygen species (ROS) fluorescence probe was used to detect intracellular ROS, and mitochondrial membrane potential JC-1 was detected by flow cytometry. The mRNA levels of caspase-3 and caspase-9 in cardiomyocytes were detected by RT-PCR. Results The cell viability of the hypoxia-reoxygenation group was significantly lower than control group (P ＜ 0.01). The cell viability of the hypoxia-reoxygenation + Irisin group was higher than hypoxia-reoxygenation group (P ＜ 0.05). The intracellular ROS level in the hypoxia-reoxygenation group was higher than that in the control group (P ＜ 0.01). The level of ROS in the hypoxia-reoxygenation + Irisin group was lower than that of the hypoxia-reoxygenation group (P ＜ 0.05). The mitochondrial membrane potential JC-1 level in hypoxia-reoxygenation group was lower than control group (P ＜ 0.05). The level of mitochondrial membrane potential JC-1 in hypoxia-reoxygenation + Irisin group was higher than hypoxia-reoxygenation group (P ＜ 0.05). The mRNA levels of caspase-3 and caspase-9 in the hypoxia-reoxygenation group were higher than the control group (P ＜ 0.05). The mRNA levels of caspase-3 and caspase-9 in hypoxia-reoxygenation + Irisin group were lower than hypoxia-reoxygenation group (P ＜ 0.05). Conclusion Irisin can significantly improve the cell viability of cardiomyocytes after hypoxia-reoxygenation, reduce ROS production, restore mitochondrial membrane potential, and inhibit apoptosis pathway. It can be used as a potential therapeutic agent for improving myocardial ischemia-reperfusion injury.

Key words： Hypoxia-reoxygenation H9C2 Reactive exygen species Myocardial injury Apoptosis

基金资助:国家自然科学基金面上资助项目（81870172、81 470438）；
陕西省重点研发计划项目（2018SF-129、2018ZDXM-SF-068、2018SF-114）。

通讯作者: 于军（1974.10-），男，博士，教授，硕士生导师；研究方向：心肌病的基础研究。

作者简介: 吴娟（1978.5-），女，硕士，副主任医师；研究方向：结构性心肌病的临床和基础。

引用本文:

吴娟1 张晓萌1 常盼1 朱肖星2 李静1 王西辉1 王建榜1 于军3 . Irisin对H9C2心肌细胞缺氧复氧损伤后的保护作用[J]. 中国医药导报, 2019, 16(30): 7-11.
WU Juan1 ZHANG Xiaomeng1 CHANG Pan1 ZHU Xiaoxing2 LI Jing1 WANG Xihui1 WANG Jianbang1 YU Jun3. Protective effect of Irisin on damage of H9C2 cardiomyocytes under hypoxia-reoxygenation. 中国医药导报, 2019, 16(30): 7-11.

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