Panax notoginseng saponins inhibit ischemia-induced apoptosis by activating PI3K/Akt pathway in cardiomyocytes

被引：193

作者：

Chen, Shaoxian ^{[1
,2
]}

Liu, Juli ^{[1
,2
]}

Liu, Xiaoying ^{[1
]}

Fu, Yongheng ^{[1
]}

Zhang, Mengzhen ^{[1
]}

Lin, Qiuxiong ^{[1
]}

Zhu, Jiening ^{[1
]}

Mai, Liping ^{[1
]}

Shan, Zhixin ^{[1
]}

Yu, Xiyong ^{[1
]}

Yang, Min ^{[1
,3
]}

Lin, Shuguang

机构：

[1] Guangdong Acad Med Sci, Guangdong Gen Hosp, Med Res Ctr, Guangzhou 510080, Guangdong, Peoples R China

[2] Shantou Univ, Coll Med, Shantou 515041, Peoples R China

[3] Guangdong Acad Med Sci, Guangdong Gen Hosp, Dept Pharm, Guangzhou 510080, Guangdong, Peoples R China

来源：

JOURNAL OF ETHNOPHARMACOLOGY | 2011年 / 137卷 / 01期

关键词：

Panax notoginseng saponins; Apoptosis; Ischemia; Akt; p-Akt; MYOCARDIAL-INFARCTION; HEART-DISEASES; IN-VITRO; AKT; REPERFUSION; SURVIVAL; MITOCHONDRION; OPPORTUNITIES; THERAPEUTICS; INJURY;

D O I：

10.1016/j.jep.2011.05.011

中图分类号：

Q94 [植物学];

学科分类号：

071001 [植物学];

摘要：

Aim of this study: The panax notoginseng saponins (PNS) have been clinically used for the treatment of cardiovascular diseases and stroke in China. Evidences demonstrated that PNS could protect cardiomyocytes from injury induced by ischemia, but the underlying molecular mechanisms of this protective effect are still unclear. This study was aimed to investigate the protective effect and potential molecular mechanisms of PNS on apoptosis in H9c2 cells in vitro and rat myocardial ischemia injury model in vivo. Materials and methods: H9c2 cells subjected to serum, glucose and oxygen deprivation (SGOD) were used as in vitro models and SD rats subjected to left anterior descending (LAD) coronary artery ligation were used as in vivo models. The anti-apoptotic effect of PNS was evaluated by Annexin V/PI analysis or TUNEL assay. Mitochondrial membrane potential (Delta psi m) was detected by JC-1 analysis. The expression of Akt and phosphorylated Akt (p-Akt) were detected by western blot assay. Results: PNS exhibited anti-apoptotic effect both in H9c2 cells and in ischemic myocardial tissues. However, the effect was blocked in vitro by LY294002, a specific PI3k inhibitor. The anti-apoptotic effect of PNS was mediated by stabilizing Delta psi m in H9c2 cells. Furthermore the indices of the left ventricular ejection fractions (EF), left ventricular fractional shortening (FS), left ventricular dimensions at end diastole (LVDd) and left ventricular dimensions at end systole (LVDs) suggested that PNS improved rats cardiac function. PNS significantly increased p-Akt both in H9c2 cells and in ischemic myocardial tissues and this effect was also blocked by LY294002 in H9c2 cells. Conclusion: Results of this study suggested that PNS could protect myocardial cells from apoptosis induced by ischemia in both the in vitro and in vivo models through activating PI3K/Akt signaling pathway. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

引用

页码：263 / 270

页数：8

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