Effects of N-acetylcysteine on caveolin-3 expression during myocardial ischemia-reperfusion in diabetic rats

Objective To evaluate the effects of N-acetycysteine on the expression of caveolin-3 (Cav-3) during myocardial ischemia-reperfusion (I/R) in diabetic rats. Methods Twenty-four pathogen-free healthy adult male Sprague-Dawley rats, weighing 230-270 g, were divided into 3 groups (n=8 each) using a random number table: myocardial I/R group (group I/R), diabetes mellitus plus myocardial I/R group (group D) and N-acetycysteine group (group NAC). Diabetes mellitus was induced by injection of streptozotocin 60 mg/kg via the tail vein and confirmed by blood glucose ≥16.7 mmol/L 3 days later.At 1 week after successful establishment of the model, N-acetycysteine 1.5 g·kg-1·d-1 was injected through a gastric tube into stomach for 4 consecutive weeks in group NAC, and the equal volume of normal saline was given for 4 consecutive weeks in I/R and D groups.Myocardial I/R was then induced by 30 min ligation of the left anterior descending branch of the coronary artery followed by 2 h of reperfusion.At the end of reperfusion, the myocardial infarct size was determined by triphenyl tetrazolium chloride staining, the levels of serum creatine kinase-MB (CK-MB) and 15-F2t-Isoprostane were measured by enzyme-linked immunosorbent assay, and the expression of myocardial Cav-3, Akt, phosphor-Akt (p-Akt), endothelial nitric oxide synthase (eNOS) and phosphor-eNOS (p-eNOS) was detected by Western blot. Results Compared with group I/R, the myocardial infarct size and levels of serum CK-MB and 15-F2t-Isoprostane were significantly increased, and the myocardial Cav-3, p-Akt and p-eNOS expression and NO level were decreased in group D (P<0.05). Compared with group D, the myocardial infarct size and levels of serum CK-MB and 15-F2t-Isoprostane were significantly decreased, and the myocardial Cav-3, p-Akt and p-eNOS expression and NO level were increased in group NAC (P<0.05). Conclusion N-acetycystein can activate Akt/eNOS/NO signaling pathway through up-regulating myocardial Cav-3 expression, thus reducing myocardial I/R injury in diabetic rats. Key words: N-acetylcysteine; Diabetes mellitus; Myocardial reperfusion injury; Coated pits, cell-membrane