Open AccessThe Effect of High Intensity Aerobic Exercise on Levels of Galectin-3 and Protein Kinase C in Diabetic Male Rats
Author(s) -
Abolfazl Samiei,
Naser Behpoor,
Vahid Tadibi,
Rozita Fathi
Publication year - 2020
Publication title -
taḥqīqāt-i bālīnī dar ̒ulūm-i pīrāpizishkī
Language(s) - English
Resource type - Journals
eISSN - 2345-3338
pISSN - 2322-1593
DOI - 10.5812/jcrps.80362
Subject(s) - medicine , diabetes mellitus , streptozotocin , aerobic exercise , analysis of variance , endocrinology , treadmill , fibrosis , cardiac function curve , diabetic cardiomyopathy , heart failure , cardiomyopathy
Background: Cardiac fibrosis is one of the complications of diabetes. Physical activity may be effective in reducing cardiac fibrosis through affecting hyperglycemia. Objectives: Accordingly, the purpose of this study was to investigate the effect of high intensity aerobic exercise on levels of galectin-3 and protein kinase C in diabetic rats. Methods: In this study, 30 male wistar rats were randomly divided into 3 groups (control, diabetic control and exercise diabetic). The induction of diabetes was performed by intraperitoneally injected streptozotocin solution at a dose of 55 mg/kg of body weight. The training program included 8 weeks of treadmill running for 60 minutes and a speed of 34 m/min. Subjects in all experimental groups (48 hours after the last training session) were anesthetized and then the heart tissue was isolated from the aortic root area. Data analysis was performed using one-way ANOVA and Tukey’s post hoc test to determine the difference between the groups. Results: The results showed that galectin-3 and PKC had a significant increase in the diabetics control group compared to the healthy group. It was also found that endurance training with high intensity caused a significant decrease in galectin-3 and PKC compared to diabetic control group. Conclusions: It seems that endurance training in diabetes is an effective method for decreasing the activity of signaling cascade of the pathway of pathogenesis of fibrosis in the heart of diabetic rats.