Page 31 - 南京医科大学学报自然科学版

第42卷第11期 南京医科大学学报（自然科学版）
2022年11月 Journal of Nanjing Medical University（Natural Sciences） ·1523 ·

·基础研究·

球形脂联素对间歇低氧所致H9C2细胞损伤的保护作用及机制

丁文筱 ，张 蔷 ，丁 宁 ，张希龙 ，董艳彬 3*
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1 东南大学附属中大医院呼吸与危重症医学科，江苏 南京 210009；南京医科大学第一附属医院呼吸与危重症医学科，急诊
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科，江苏 南京 210029
［摘 要］ 目的：探讨Parkin介导的线粒体自噬在球形脂联素（globular adiponectin，gAPN）减轻间歇低氧（intermittent hypoxia，
IH）所致H9C2心肌细胞损伤中的作用及相关机制。方法：建立H9C2细胞IH模型来模拟阻塞性睡眠呼吸暂停低通气综合征。
采用流式细胞术检测细胞凋亡。采用JC⁃1试剂盒检测线粒体膜电位（mitochondrial membrane potential，MMP）。采用免疫印迹
法检测Parkin、Bax、Bcl⁃2蛋白表达。采用Parkin siRNA抑制Parkin基因表达。采用LC3与线粒体红色荧光探针进行荧光共定
位检测线粒体自噬。结果：IH暴露后，H9C2细胞凋亡率、Bax及Parkin蛋白表达水平、线粒体自噬明显升高，MMP下降，Bcl⁃2
蛋白表达水平下降；给予 gAPN 保护后，IH+gAPN 组细胞凋亡率、Bax 蛋白表达水平较 IH 组下降，MMP 较 IH 组升高，Bcl⁃2 及
Parkin蛋白表达水平、线粒体自噬也较IH组升高。抑制Parkin基因表达后，线粒体自噬明显下降，线粒体损伤、心肌细胞凋亡
率明显增加。结论：gAPN通过上调Parkin介导的线粒体自噬减轻IH所致H9C2心肌细胞损伤。
［关键词］ 阻塞性睡眠呼吸暂停低通气综合征；球形脂联素；线粒体自噬；间歇低氧
［中图分类号］ R563.9 ［文献标志码］ A ［文章编号］ 1007⁃4368（2022）11⁃1523⁃08
doi：10.7655/NYDXBNS20221104

Effects and mechanisms of globular adiponectin on intermittent hypoxia induced H9C2

cell injury
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DING Wenxiao ，ZHANG Qiang ，DING Ning ，ZHANG Xilong ，DONG Yanbin
Department of Pulmonary and Critical Care Medicine，Zhongda Hospital，Medical School，Southeast University，
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Nanjing 210009；Department of Pulmonary and Critical Care Medicine，Department of Emergency，the First
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Affiliated Hospital of Nanjing Medical University，Nanjing 210029，China

［Abstract］ Objective：This study aims to evaluate the effect of Parkin mediated mitophagy on globular adiponectin（gAPN）
ameliorated H9C2 cardiomyocytes injury induced by intermittent hypoxia（IH）and the potential mechanisms. Methods：The cell IH
model was established. H9C2 cell apoptosis was detected by flow cytometry. The mitophagy was detected by fluorescence colocalization
of LC3 and mitochondrial red marker. The protein expression levels of Bax，Bcl⁃2 and Parkin were detected by Western blot. The
mitochondrial membrane potential（MMP） was detected by JC ⁃ 1 kit. Results：After IH exposure，the apoptosis of H9C2
cardiomyocytes，protein expression levels of Bax and Parkin，mitophagy were increased，MMP and Bcl ⁃ 2 protein expression were
decreased. After gAPN treatment，the apoptosis of H9C2 cardiomyocytes，Bax protein expression level were decreased，the MMP，
protein expression levels of Bcl ⁃ 2 and Parkin，and mitophagy were increased. Inhibiting Parkin gene expression decreased the
mitophagy，and increased the mitochondrial injury and H9C2 cell apoptosis. Conclusion：gAPN ameliorated the IH induced H9C2
cardiomyocytes injury through upregulating Parkin mediated mitophagy.
［Key words］ obstructive sleep apnea hypopnea syndrome；globular adiponectin；mitophagy；intermittent hypoxia
［J Nanjing Med Univ，2022，42（11）：1523⁃1529，1538］

阻塞性睡眠呼吸暂停低通气综合征（obstruc⁃
［基金项目］ 国家自然科学基金项目（81700090，81770086） tive sleep apnea hypopnea syndrome，OSAHS）是由于
∗ 睡眠期间反复出现上气道的完全或部分坍陷，引起
通信作者（Corresponding author），E⁃mail：dybbin@163.com