Effect of sleep deprivation on caveolin-3 expression and apoptosis in the themyocardium after ischemia/reperfusion
Objective:To investigate the effects of sleep deprivation on the expression of myocardial caveo-lin-3(Cav-3)and apoptosis after ischemia/reperfusion(I/R).Methods:The acute sleep deprivation model of mouse was established by using the improved multi platform water environment method.Af-ter four days of sleep deprivation,the myocardial I/R model was established by ligating the left anteri-or descending coronary artery of mice for 45 minutes,and then reperfusion for 120 minutes.Hematox-ylin eosin staining was used to observe the pathological changes of mouse myocardium,TTC staining was used to determine the myocardial infarction area of mice after I/R,ELASA method was used to measure the content of serum creatine kinase isoenzyme(CK-MB),deoxyribonucleotidyltransferase mediated dUTP nick end labeling(TUNEL)method was used to detect apoptosis,and Western Blot method was used to detect the expression level of Cleaved caspase-3 and Cav-3.Results:Compared with the mice in control group,the mice became irritable and irritated after four days of sleep depriva-tion.Pathological observation showed that the arrangement of myocardial tissue fibers was disordered after sleep deprivation.Further research found that the content of CK-MB in plasma and the level of apoptosis of myocardial cells in mice after sleep deprivation were significantly increased(TUNEL staining positive cells and the level of Cleaved caspase-3 were significantly increased),while the level of expression of Cav-3 in myocardium was significantly reduced.After sleep deprived mice suffered further myocardial I/R,and their myocardial infarction area,CK-MB content and apoptosis level in-creased,while the expression of Cav-3 decreased(P<0.05).Conclusion:Sleep deprivation can make myocardium more resistant to ischemia reperfusion injury,and its mechanism may be related to the down-regulation of Cav-3 expression and excessive activation of myocardial cell apoptosis.