Role of AMP-activated protein kinase in hydrogen sulfide postconditioning protecting on type 2 diabetic rats with myocardial ischemia reperfusion injury
- VernacularTitle:AMPK通路在硫化氢后处理减轻2型糖尿病大鼠心肌缺血-再灌注损伤中的作用
- Author:
Bo SUN
;
Chen WANG
;
Wenjie ZHAO
;
Shigang QIAO
- Keywords:
AMP-activated protein kinase;
Hydrogen sulfide;
Myocardial ischemia/reperfu-sion;
Type 2 diabetes mellitus;
Autophagy
- From:
The Journal of Clinical Anesthesiology
2017;33(9):881-884
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of hydrogen sulfide (H 2 S or NaHS)on myo-cardial ischemia reperfusion injury induced in type 2 diabetic rats in vivo and the role of AMP-activated protein kinase (AMPK)signal pathway.Methods The induced type 2 diabetic rat models were anesthetized,left thoracotomy were performed.All the models were randomly divided into six groups (n = 14):group Sham;group IR:the left anterior descending artery was ligated 30 min, reperfused for 4 hours;group CC:prior to thoracotomy,compound c was intraperitoneally injected 250 μg/kg,then received the same treatment as group IR;group DMSO received the same treatment as compound c group but DMSO was injected intraperitoneally as control;group NaHS:the left ante-rior descending artery was injected NaHS 0.05 mg/kg then reperfused for 4 hours;group CC +NaHS:prior to thoracotomy,compound c was intraperitoneally injected 250 μg/kg,then NaHS 0.05 mg/kg injected intravenously and reperfused 4 hours.All the rat models euthanatized,infarcted area was detected by TTC assay.The AMPK,LC3 and p62 were analyzed by Western blot.Results Com-pared with group Sham,the infarcted area and concentration of AMPK,LC3 and p62 were increased in other groups (P <0.05).Compared with group IR,the infarcted area and concentration of LC3, p62 markablely decreased in group NaHS (P < 0.05 ).Compared with group NaHS,the infarcted area and concentration of LC3,p62 significantly increased but AMPK down-regulated in group CC+NaHS (P <0.05).Conclusion Hydrogen sulfide could alleviate myocardial infraction via AMPK sig-nal pathway in type 2 diabetic rats'IR models.