[Effects of hydrogen-rich saline on endoplasmic reticulum stress during myocardial ischemia-reperfusion in rats].

ABSTRACT

OBJECTIVE: To explore the effects of hydrogen-rich saline on endoplasmic reticulum stress during myocardial ischemia-reperfusion (I/R) in rats. METHODS: A total of 150 healthy male Sprague-Dawley rats were selected and then randomly divided into 5 groups of normal control (I), sham operation (II), myocardial ischemia-reperfusion (III), hydrogen-rich saline (IV) and normal saline (V) (n = 30 each). Group I had no treatment. In group II, anterior descending branch was merely exposed but not ligated. Myocardial I/R was induced by an occlusion of anterior descending branch of left coronary artery for 30 min followed by 12 h and 24 h of reperfusion with bimbaum. Hydrogen-rich saline 1 ml/100 g was injected intraperitoneally 5 min before reperfusion in group IV. Normal saline 1 ml/100 g was injected intraperitoneally 5 min before reperfusion in group V. The rats were sacrificed at 12 h and 24 h of reperfusion and heart tissues harvested. The pathological changes of myocardial tissue were detected by hematoxylin & eosin staining. The apoptotic cardiomyocytes of myocardial tissue were tested by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). And the expressions of GRP78, Caspase-12, Bcl-2 and Bax in myocardial tissue were detected by Western blot. RESULTS: Compared with groups I and II, the numbers of apoptotic cardiomyocytes, the expression of GRP78, Caspase-12 and Bax in myocardial tissue significantly increased and the expression of Bcl-2 in myocardial tissue significantly decreased in groups III, IV and V. Compared with group III and V, the numbers of apoptotic cardiomyocytes, the expression of GRP78, Caspase-12 and Bax in myocardial tissue significantly decreased while the expression of Bcl-2 in myocardial tissue significantly increased in group IV. CONCLUSIONS: Hydrogen-rich saline may decrease cell apoptosis and attenuate myocardial reperfusion injury through inhibiting endoplasmic reticulum stress. The mechanism may be associated with decreasing the expression of GRP78, Caspase-12 and Bax and increasing the expression of Bcl-2 in myocardial tissue.