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冬青皂苷A通过抗凋亡途径减轻缺血再灌注诱导的心肌损伤。

Ilexsaponin A attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway.

作者信息

Zhang Shuang-Wei, Liu Yu, Wang Fang, Qiang Jiao, Liu Pan, Zhang Jun, Xu Jin-Wen

机构信息

The second affiliated hospital of Guangzhou Medical University, Changgang east road, Guangzhou, China.

School of Chinese Pharmaceutical Science, Guangzhou University of Chinese Medicine, University Town, Guangzhou, China.

出版信息

PLoS One. 2017 Feb 9;12(2):e0170984. doi: 10.1371/journal.pone.0170984. eCollection 2017.

DOI:10.1371/journal.pone.0170984
PMID:28182689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5300190/
Abstract

The protective effects of ilexsaponin A on ischemia-reperfusion-induced myocardial injury were investigated. Myocardial ischemia/reperfusion model was established in male Sprague-Dawley rats. Myocardial injury was evaluated by TTC staining and myocardial marker enzyme leakage. The in vitro protective potential of Ilexsaponin A was assessed on hypoxia/reoxygenation cellular model in neonatal rat cardiomyocytes. Cellular viability and apoptosis were evaluated by MTT and TUNEL assay. Caspase-3, cleaved caspase-3, bax, bcl-2, p-Akt and Akt protein expression levels were detected by western-blot. Ilexsaponin A treatment was able to attenuate the myocardial injury in ischemia/reperfusion model by reducing myocardial infarct size and lower the serum levels of LDH, AST and CK-MB. The in vitro study also showed that ilexsaponin A treatment could increase cellular viability and inhibit apoptosis in hypoxia/reoxygenation cardiomyocytes. Proapoptotic proteins including caspase-3, cleaved caspase-3 and bax were significantly reduced and anti-apoptotic protein bcl-2 was significantly increased by ilexsaponin A treatment in hypoxia/reoxygenation cardiomyocytes. Moreover, Ilexsaponin A treatment was able to increase the expression levels of p-Akt in hypoxia/reoxygenation cellular model and myocardial ischemia/reperfusion animal model. Coupled results from both in vivo and in vitro experiments indicate that Ilexsaponin A attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway.

摘要

研究了冬凌草皂苷A对缺血再灌注诱导的心肌损伤的保护作用。在雄性Sprague-Dawley大鼠中建立心肌缺血/再灌注模型。通过TTC染色和心肌标志物酶泄漏评估心肌损伤。在新生大鼠心肌细胞的缺氧/复氧细胞模型上评估冬凌草皂苷A的体外保护潜力。通过MTT和TUNEL法评估细胞活力和凋亡。通过蛋白质印迹法检测Caspase-3、裂解的Caspase-3、bax、bcl-2、p-Akt和Akt蛋白表达水平。冬凌草皂苷A治疗能够通过减小心肌梗死面积和降低血清LDH、AST和CK-MB水平来减轻缺血/再灌注模型中的心肌损伤。体外研究还表明，冬凌草皂苷A治疗可增加缺氧/复氧心肌细胞的细胞活力并抑制凋亡。冬凌草皂苷A处理可使缺氧/复氧心肌细胞中包括Caspase-3、裂解的Caspase-3和bax在内的促凋亡蛋白显著降低，抗凋亡蛋白bcl-2显著增加。此外，冬凌草皂苷A处理能够增加缺氧/复氧细胞模型和心肌缺血/再灌注动物模型中p-Akt的表达水平。体内和体外实验的联合结果表明，冬凌草皂苷A通过抗凋亡途径减轻缺血再灌注诱导的心肌损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/b75380400c48/pone.0170984.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/d11e0af04e65/pone.0170984.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/9446ae8c8cce/pone.0170984.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/3f66a75b991c/pone.0170984.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/62df1296cd31/pone.0170984.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/b75380400c48/pone.0170984.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/d11e0af04e65/pone.0170984.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/9446ae8c8cce/pone.0170984.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/3f66a75b991c/pone.0170984.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/62df1296cd31/pone.0170984.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d01f/5300190/b75380400c48/pone.0170984.g005.jpg

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