Effect Of Aerobic Exercise On Cardiac Diastolic Dysfunction: Role Of Heat Shock Protein 27

Abstract

PURPOSE: To evaluate the role of heat shock protein 27 (HSP27) in the effect of aerobic exercise on cardiac diastolic dysfunction in type 2 diabetic rats. METHODS: Forty male Sprague-Dawley rats were randomly divided into four groups: control (C), aerobic exercise (A), diabetes (D), and diabetes plus aerobic exercise (DA). Type 2 diabetes was induced by feeding with a high-fat high-sugar diet for 7 weeks followed by a single intraperitoneal injection of streptozotocin (30mg/kg) in the rats. Aerobic exercise was performed on a rodent treadmill at 21m/min for 60 min, 5 days per week for 8 weeks. Metabolic factors, such as fasting blood glucose (FBG), triglycerides (TG), cholesterol (CHOL) and lipoproteins, were determined by a standard procedure. Cardiac structure and function, such as left ventricular diastolic upper diameter (LVIDd), left ventricular diastolic terminal volume (EDV) and ejection fraction (EF), were measured using echocardiography. Myocardial HSP27 protein expression and phosphorylation were determined using western blot, and myocardial HSP27-titin colocalization were determined using double immunofluorescence. Two-way ANOVAs with post-hoc tests were used to assess differences between groups. RESULTS: No pathological changes were observed in the myocardial structure in all four groups. Compared to the C group, the D group had significantly higher levels of FBG, TG, and CHOL (all p<0.01), and significantly lower LVIDd and EDV (both p<0.01). Compared to the D group, the DA group had significantly lower levels of FBG, TG, and CHOL (all p<0.01) and significantly higher LVIDd and EDV (both p<0.05). Interestingly, compared to the C group, the D group showed significantly lower myocardial HSP27 phosphorylation and HSP27-titin colocalization (both p<0.05), while the DA group showed significantly higher myocardial HSP27 protein expression and phosphorylation, and HSP27-titin colocalization than the D group (all p<0.01). CONCLUSION: Decreases in myocardial HSP27 phosphorylation and HSP27-titin colocalization are likely involved in early diastolic dysfunction in diabetic rats. Increased HSP27 phosphorylation and titin colocalization may be an important mechanism by which aerobic exercise restores diastolic function in diabetic rats.