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来自[具体来源未提及]的内酯成分通过抑制自噬减轻心肌缺血损伤。

Lactone Component From Alleviates Myocardial Ischemia Injury Through Inhibiting Autophagy.

作者信息

Wang Gang, Dai Guoliang, Song Jie, Zhu Maomao, Liu Ying, Hou Xuefeng, Ke Zhongcheng, Zhou Yuanli, Qiu Huihui, Wang Fujing, Jiang Nan, Jia Xiaobin, Feng Liang

机构信息

College of Traditional Chinese Medicine, China Pharmaceutical University, Nanjing, China.

College of Pharmacy, Anhui University of Chinese Medicine, Hefei, China.

出版信息

Front Pharmacol. 2018 Mar 29;9:301. doi: 10.3389/fphar.2018.00301. eCollection 2018.

DOI:10.3389/fphar.2018.00301
PMID:29651246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5884868/
Abstract

The dysregulation of autophagy is associated with a series of cardiovascular diseases, such as myocardial ischemia injury. Lactone component from (LLC) is the major constituent of the traditional Chinese herb Hort., which has been reported to hold potential cardioprotective effects. In this study, to determine whether LLC protects the heart through regulation of autophagy, we explored the effects of LLC on cardioprotection and autophagy in myocardial ischemia injured rats and H9c2 cardiomyocytes. Our results showed that LLC significantly reduced infarct size and serum levels of lactate dehydrogenase, creatine kinase, and cardiac troponin and ameliorated histological features in a dose-dependent manner. Similar protections were observed in cardiomyocytes subjected to oxygen-glucose deprivation (OGD). Meanwhile, LLC inhibited autophagy induced by myocardial ischemia injury, characterized by increased autophagic vacuoles, LC3-II/LC3-I ratio and the expression of Beclin 1, whereas decreased the expression of p62. Additionally, LLC combined with a lysosomal inhibitor chloroquine (CQ) reduced LC3-II/LC3-I ratio in cardiomyocytes compared with CQ alone. Furthermore, LLC-afforded cardioprotection was abolished by a specific PI3K inhibitor LY294002. Collectively, these findings demonstrated that cardioprotective effects of LLC were related to restoration of autophagic flux through the activation of PI3K/Akt/mTOR signaling pathway.

摘要

自噬失调与一系列心血管疾病相关，如心肌缺血损伤。来自[具体植物名称]的内酯成分（LLC）是传统中药[具体植物名称]的主要成分，据报道具有潜在的心脏保护作用。在本研究中，为了确定LLC是否通过调节自噬来保护心脏，我们探讨了LLC对心肌缺血损伤大鼠和H9c2心肌细胞心脏保护及自噬的影响。我们的结果表明，LLC以剂量依赖的方式显著减小梗死面积，并降低血清乳酸脱氢酶、肌酸激酶和心肌肌钙蛋白水平，改善组织学特征。在经历氧糖剥夺（OGD）的心肌细胞中也观察到类似的保护作用。同时，LLC抑制心肌缺血损伤诱导的自噬，其特征为自噬空泡增加、LC3-II/LC3-I比值及Beclin 1表达增加，而p62表达降低。此外，与单独使用溶酶体抑制剂氯喹（CQ）相比，LLC联合CQ可降低心肌细胞中LC3-II/LC3-I比值。此外，特异性PI3K抑制剂LY294002可消除LLC提供的心脏保护作用。总的来说，这些发现表明LLC的心脏保护作用与通过激活PI3K/Akt/mTOR信号通路恢复自噬流有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e80/5884868/a26a1ef5802c/fphar-09-00301-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e80/5884868/7a087b96e607/fphar-09-00301-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e80/5884868/eaa840029f74/fphar-09-00301-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e80/5884868/a26a1ef5802c/fphar-09-00301-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e80/5884868/7a087b96e607/fphar-09-00301-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e80/5884868/979057a414a0/fphar-09-00301-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e80/5884868/8d660634c5f2/fphar-09-00301-g003.jpg
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