Effect of limb ischemic preconditioning on immature myocardial cells apoptosis and endopasmic reticulum stress
10.3969/j.issn.2095-4344.2014.20.008
- VernacularTitle:下肢缺血预处理对未成熟心肌细胞凋亡和内质网应激的影响
- Author:
Zhongdong SUN
;
Yue SONG
;
Guodong LIU
;
Jie ZHANG
;
Jianwei ZHENG
- Publication Type:Journal Article
- Keywords:
lower extremity;
ischemic preconditioning;
myocytes,cardiac;
apoptosis;
endoplasmic reticulum
- From:
Chinese Journal of Tissue Engineering Research
2014;(20):3153-3157
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:In recent years, endoplasmic reticulum stress-caused apoptosis plays a crucial role in ischemia impairment and has become the hotspot of studies addressing myocardial ischemia/reperfusion (I/R) injury. The lower limb ischemic preconditioning (LIP) has the obvious protective effect on the immature myocardium, but until now, no study reports whether LIP effects on endoplasmic reticulum stress apoptosis in immature myocardial cells. OBJECTIVE:To investigate the effect of LIP on endoplasmic reticulum stress and apoptosis.
METHODS:Langendorff-perfused isolated rabbit hearts were used in this study. Twenty-four immature rabbits were randomized into three groups. Control group:Isolated rabbit heart was only perfused with Krebs-Henseleit for 180 minutes. I/R group:Isolated rabbit heart was perfused 20 minutes, and then ischemia for 60 minutes fol owed by reperfusion 100 minutes. LIP group:Limbs were repeatedly obstructed 5 minutes and relaxed 5 minutes for three times, to establish Langendorff models, and then repeated the method of ischemia/reperfusion in I/R group. The myocardial apoptosis was assayed with TUNEL method. The expression of glucose-regulated protein 78, Bcl-2, Bax and Fas was detected with western blot analysis.
RESULTS AND CONCLUSION:Compared with I/R group, apoptosis rate was significantly lower, the expression of Bcl-2 was significantly higher, and the expression of glucose-regulated protein 78, Bax and Fas was significantly lower in LIP group. This study demonstrated that LIP regulates myocardial cellapoptosis through reducing the expression of endopasmic reticulum stress GRP78, Bax and Fas and increasing the expression of Bcl-2.
