CO Inhaled Has Beneficial Effects On Cardiac Ischemia-reperfusion Injury And Suppressed The Expression Of CHOP In The Heart

Objective:Carbon monoxide (CO) is postulated to protect tissues against several types of injuries. but the precise mechanisms remain to be established. We investigated the role of CO in amelioration of cardiac ischemia–reperfusion injury in vivo and the mechanisms of antiapoptotic involved in it.Methods: myocardial ischemia-reperfusion was induced by occluding the left anterior descending coronary artery for 30 minutes. 40 rabbits were divided into 4 groups(each group,n=10) : first group is Sham group, which is suffered surgical operation except occluding the left anterior descending coronary artery. Other groups were given myocardial I/R injury operation. Rabbits except for sham group inhaled CO (250 ppm),normal air and suffered hypoxia for 24 hours in a chamber before surgical operation. All in all,4 groups was that,Sham, I/R, CO pretreatment , and hypoxia pretreatment group.Results:The CO pretreatment group after pre-exposure to 250 ppm of CO significantly reduced the ratio of infarct areas to risk areas and suppressed the level of CK-MB,LDH and the expression of CHOP in the heart;however, low barometric pressure hypoxia (0.5 atm) did not affect them.Exposure to 250ppm CO attenuated the cytoprotection against ERS.Exogenous CO prevented endothelial apoptosis triggered by these ER inducers through suppression of C/EBP homologous protein expression,Conclusion:CO has beneficial effects on cardiac ischemia–reperfusion injury; Our findings suggest that CO renders endothelial cells resistant to ER stress by downregulating C/EBP homologous(CHOP) protein expression .exogenous CO was cytoprotective against ER stress through C/EBP homologous protein suppression induced by myocardial I/R injury .Thus, CO inhaled might be potential therapeutics in myocardial ischemia-reperfusion injury diseases associated with ER stress.