Effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase expression during myocardial ischemia-reperfusion in rats.
- Author:
Ke RAN
1
;
Zheng-guo TANG
;
Li-ping DING
;
Shuang-feng LI
;
Ye-tian CHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Disease Models, Animal; Glutathione Transferase; metabolism; Hydrogen Sulfide; administration & dosage; therapeutic use; Ischemic Preconditioning, Myocardial; Male; Myocardial Reperfusion Injury; enzymology; pathology; therapy; Myocardium; enzymology; ultrastructure; Rats; Rats, Sprague-Dawley
- From: Journal of Zhejiang University. Medical sciences 2011;40(5):535-539
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of hydrogen sulfide-induced delayed preconditioning on glutathione S-transferase (GST) expression during myocardial ischemia-reperfusion in rats.
METHODSSprague-Dawley male rats were randomly divided into 4 groups (n= 10 in each): Group S (sham operation group), Group IR (ischemia/reperfusion group), Group H (IR+ NaHS 0.05 mg/kg iv, 24 h before ischemia) and Groups D receiving IR+NaHS 24 h before ischemia and 5-hydroxydecanoate (5-HD)15 min before ischemia. Animals in groups IR, H and D were subjected to ischemia by 30 min of coronary artery occlusion followed by 2 h of reperfusion. At the end of the reperfusion, myocardial infarct size (IS) was examined. Glutathione S-transferase (GST) was measured by Western blotting. The myocardial ultrastructures were observed under the electron microscopy.
RESULTSThe IS was significantly smaller in Group H than that in Group IR [(25.40 ± 3.54)% compared with (38.27 ± 5.64)%, P<0.05]. The GST expression in myocardium was significantly higher in Group H than that in Group IR. Microscopic examination showed less myocardial damage in Group H than in Group IR. The protective effects of delayed preconditioning by hydrogen sulfide was prevented by 5-HD pre-treatment.
CONCLUSIONThe hydrogen sulfide-induced delayed preconditioning attenuates myocardial IR injury possibly through up-regulating glutathione S-transferase expression in rats.