title: [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.
authors.affiliation: Department of Cardiology, Daqing Oil Field General Hospital, Daqing 163001, China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Cardiology, Daqing Oil Field General Hospital, Daqing 163001, China.
authors.forename: Yulong
authors.initials: Y
authors.lastname: Tang
authors.affiliation: Department of Cardiology, Daqing Oil Field General Hospital, Daqing 163001, China.
authors.forename: Chuantao
authors.initials: C
authors.lastname: Suo
authors.affiliation: Department of Cardiology, Daqing Oil Field General Hospital, Daqing 163001, China.
authors.forename: Dayi
authors.initials: D
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Daqing Oil Field General Hospital, Daqing 163001, China.
authors.forename: Shiyang
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Cardiology, Daqing Oil Field General Hospital, Daqing 163001, China. Email: 791685879@qq.com.
authors.forename: Hui
authors.initials: H
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis; D053454:Caspase 12; D059865:Endoplasmic Reticulum Stress; D006859:Hydrogen; D007511:Ischemia; D008297:Male; D015428:Myocardial Reperfusion Injury; D019253:Proto-Oncogene Proteins c-bcl-2; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride; D051028:bcl-2-Associated X Protein
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D012965:Sodium Chloride; D006859:Hydrogen; C506443:Casp12 protein, rat; D053454:Caspase 12