Effects of diazoxide on Fas/FasL protein expressions in rat myocardium suffered from long-term hypothermic preservation.
- Author:
Ying FAN
1
;
Ming-Zhi ZHENG
;
Wei GUO
;
Jian-Ping JIANG
;
Li ZHU
;
Yue-Liang SHEN
;
Ying-Ying CHEN
Author Information
1. Department of Physiology, School of Medicine, Zhejiang University, Hangzhou 310058, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Cryopreservation;
Decanoic Acids;
pharmacology;
Diazoxide;
pharmacology;
Fas Ligand Protein;
metabolism;
Heart;
drug effects;
Hydroxy Acids;
pharmacology;
Myocardium;
metabolism;
Myocytes, Cardiac;
cytology;
drug effects;
Potassium Channel Blockers;
pharmacology;
Potassium Channels;
Rats;
fas Receptor;
metabolism
- From:
Acta Physiologica Sinica
2008;60(1):11-16
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to investigate the effect of a mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) opener, diazoxide (DE), on Fas/FasL protein expressions in rat heart suffered from long-term hypothermic preservation. The Langendorff isolated rat heart model was used. The hearts were stored in 4 °C Celsior solution with or without (control) DE for 8 h followed by 60 min of reperfusion. The recovery of rate-pressure product (RPP) was observed. Apoptotic cardiomyocytes were detected by TdT-mediated dUTP nick end labeling (TUNEL) technique. The expressions of Fas/FasL proteins were also analyzed by immunohistochemical method. The results showed that compared with the control group, DE (30 mmol/L) increased the recovery of RPP during reperfusion, reduced the percentage of apoptotic cells and the expressions of Fas and FasL proteins in rat hearts suffered from 8 h of hypothermic preservation. The above effects of DE were attenuated by a mitoK(ATP) channel inhibitor 5-hydroxydecanoate (5-HD). These results indicate that DE could alleviate rat myocardial injury induced by ischemia-reperfusion through reducing the expressions of Fas and FasL proteins via opening of mitoK(ATP)channel.
