| Abstract: | Impaired expression of heat shock proteins (HSP s) and increased oxidative stress may contribute to the pathophysiology of diabetes by disrupted tissue protection. Acute exercise induces oxidative stress, whereas exercise training up‐regulates endogenous antioxidant defenses and HSP expression. Although diabetic nephropathy is a major contributor to diabetic morbidity, information regarding the effect of HSP s on kidney protection is limited. This study evaluated the effects of eight‐week exercise training on kidney HSP expression and markers of oxidative stress at rest and after acute exercise in rats with or without streptozotocin‐induced diabetes. Induction of diabetes increased DNA ‐binding activity of heat shock factor‐1, but decreased the expression of HSP 72, HSP 60, and HSP 90. The inflammatory markers IL ‐6 and TNF ‐alpha were increased in the kidney tissue of diabetic animals. Both exercise training and acute exercise increased HSP 72 and HSP 90 protein levels only in non‐diabetic rats. On the other hand, exercise training appeared to reverse the diabetes‐induced histological changes together with decreased expression of TGF ‐beta as a key inducer of glomerulosclerosis, and decreased levels of IL ‐6 and TNF ‐alpha. Notably, HSP 72 and TGF ‐beta were negatively correlated. In conclusion, impaired HSP defense seems to contribute to kidney injury vulnerability in diabetes and exercise training does not up‐regulate kidney HSP expression despite the improvements in histopathological and inflammatory markers. |
