| Adiponectin通过FoxO1信号通路减轻阿霉素细胞毒性的作用机制研究 |
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| 引用本文： | 陈亚武,金屏,王少玮,郝瑞军,刘金成,郭红. Adiponectin通过FoxO1信号通路减轻阿霉素细胞毒性的作用机制研究[J]. 心脏杂志, 2021, 33(2): 127-132. DOI: 10.12125/j.chj.202008066 |
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| 作者姓名： | 陈亚武 金屏 王少玮 郝瑞军 刘金成 郭红 |
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| 作者单位： | 1.空军军医大学西京医院心血管外科，陕西 西安 710032 |
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| 摘 要： | 目的 阐明FoxO1在脂联素(Adiponectin,APN)减轻阿霉素(Doxorubicin,DOX)心肌细胞毒性中的作用及机制.方法 将分离的乳鼠心肌原代细胞(Neonatal rat cardiomyocytes,nrCMs)随机分为对照组(CON)、APN处理组(APN)、DOX损伤组(DOX)、APN保护组...
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| 关 键 词： | 脂联素 阿霉素 FoxO1 自噬 |
| 收稿时间： | 2020-08-25 |
Protective role of Adiponectin on FoxO1-dependent autophagy against doxorubicin-induced cardiotoxicity |
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| Affiliation: | 1.Department of Cardiovascular Surgery, Xijing Hospital, Air Force Medical University, Xi’an 710032, Shaanxi, China2.Department of Cardiovascular Surgery, Fugu Renmin Hospital, Yulin 719499, Shaanxi, China |
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| Abstract: | AIM To elucidate the mechanism of foxO1 signaling pathway in the protective role of adiponectin (APN) against doxorubicin-induced cardiotoxicity. METHODS Neonatal rat cardiomyocytes (nrCMs) were randomly divided into the following groups: CON, APN, APN-DOX, DOX-Scramble siRNA, DOX-FoxO1 siRNA, APN-DOX-Scramble siRNA, and APN-DOX-FoxO1 siRNA. Cell viability was detected by CCK-8 kit, mitochondrial ATP production was detected by ATP detection kit, ROS production was detected by ROS detection kit, and autophagy marker protein expression was detected by Western blot. RESULTS Compared with CON group, DOX treatment significantly decreased cell viability and mitochondrial ATP production but increased ROS production and activated autophagy (P<0.05). APN pretreatment significantly reduced DOX induced cardiotoxicity by inhibiting autophagy. In terms of the mechanism of the protective role of APN against Dox-induced cardiotoxicity, we found that APN inhibited the activation of autophagy by up-regulating the expression of phospho FoxO1, thus protecting nrCMs cells from DOX-induced cardiotoxicity. However, the myocardial protective effect of APN was abolished by FoxO1 siRNA treatment, such as the inhibition of autophagy and ATP production, and the increase of ROS production. CONCLUSION APN attenuates DOX induced cardiotoxicity by up-regulating foxO1 phosphorylation and inhibiting autophagy activation. |
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