Hydromorphone postconditioning attenuates myocardial ischemia/reperfusion-induced apoptosis in rats through PI3K/AKT pathway
10.3760/cma.j.issn.1671-0282.2021.11.009
- VernacularTitle:氢吗啡酮后处理经PI3K/Akt通路减轻大鼠心肌缺血-再灌注细胞凋亡
- Author:
Yun WANG
1
;
Zongze ZHANG
;
Jingjing ZHANG
;
Yun WU
;
Yanlin WANG
Author Information
1. 武汉大学中南医院麻醉科 430071
- Keywords:
Ischemia/reperfusion;
Apoptosis;
Hydromorhphone;
Phosphatidylinositol-3-kinase;
Protein serine threonine kinase
- From:
Chinese Journal of Emergency Medicine
2021;30(11):1329-1333
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of PI3K/Akt signaling pathway in hydromorphone postconditioning on alleviating myocardial ischemia/reperfusion (I/R)-induced apoptosis in rats.Methods:Forty healthy male SD rats were randomly(random number) divided into five groups, with 8 rats in each group:①sham group;②I/R group;③I/R+hydromorphone group (I/R+H group);④I/R+PI3K inhibitor group (I/R+W group); and⑤I/R+hydromorphone+PI3K inhibitor group (I/R+H+W group). The myocardial ischemia/reperfusion injury model was established by ligating the left anterior descending coronary artery for 30 min and reperfusion for 120 min. After the experiment, the area of myocardial infarction was measured by 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining. The amount of serum lactate dehydrogenase (LDH) leakage was estimated by colorimetry . The cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) assay. The protein expressions of p-Akt, Bcl-2 and Bax were detected by Western blot. Comparisons among groups were carried out by analysis of variance (ANOVA).Results:Compared with the sham group, the area of myocardial infarction, serum LDH leakage and cardiomyocyte apoptosis were significantly increased, p-Akt and Bax expression were upregulated, Bcl-2 expression was downregulated in the I/R group ( P<0.05). Compared with the I/R group, the area of myocardial infarction, serum LDH leakage and cardiomyocyte apoptosis were markedly decreased, p-Akt and Bcl-2 expression were upregulated and Bax expression was downregulated in the I/R+H group ( P<0.05). Compared with the I/R+H group, the area of myocardial infarction, serum LDH leakage and cardiomyocyte apoptosis were significantly increased, p-Akt and Bcl-2 expression were downregulated, and Bax expression was upregulated in the I/R+H+W group ( P<0.05). Conclusions:Hydromorphone postconditioning can alleviate cardiomyocyte apoptosis induced by myocardial ischemia/reperfusion, and its protection mechanism may be related to the activation of PI3K/Akt signaling pathway.
