Heme oxygenase-1 pathway is involved in delayed protection induced by heat stress against cardiac ischemia-reperfusion injury.
Previous studies have shown that heme oxygenase-1 (HO-1), a heat stress protein (HSP32), has a beneficial effect on the ischemic myocardium. The purpose of the present study was to explore whether HO-1 is involved in delayed cardioprotection provided by heat stress in vivo. Sprague--Dawley rats were pretreated with whole body hyperthermia (rectal 42 degrees C) for 15 min followed by ischemia-reperfusion 24 h later. Ischemia-reperfusion injury was induced by 45 min of coronary artery occlusion followed by a 3-h reperfusion. Myocardial injury degree was evaluated by measurement of infarct size and serum creatine kinase (CK) activity. The expression of HO-1 mRNA and protein in myocardial tissues were measured. Pretreatment with hyperthemia significantly reduced infarct size and CK release during reperfusion, which was completely blocked by pretreatment with ZnPP-9, an inhibitor of HO and methylene blue, an inhibitor of soluble guanylate cyclase. Heat stress also significantly increased the expression of HO-1 mRNA and protein, and the effect was not affected by pretreatment with methylene blue. The present results suggest that the HO-1 pathway is involved in the mediation of delayed cardioprotection by heat stress in rats.
Lu
Rong
R
Department of Pharmacology, Xiang-Ya Medical College, Central South University, Changsha, Hunan 410078, China.
Peng
Jun
J
Xiao
Liang
L
Deng
Han Wu
HW
Li
Yuan Jian
YJ
D000818:Animals; D018869:Heat-Shock Response; D006419:Heme Oxygenase (Decyclizing) / Q000502:physiology*; D051547:Heme Oxygenase-1; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000201:enzymology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1