The Effects of Finasteride on Apoptosis, Antioxidants, and Cytokines in Experimental Diabetes Rats

Diabetes mellitus (DM) is one of the five leading causes of death worldwide. Finasteride is an inhibitor of type 2 5-alpha reductase enzyme. In this study, we aimed to investigate the effects of finasteride on apoptosis, oxidative stress, antioxidants, and cytokines in the liver, kidney, and testis in an experimental diabetes model in rats. Thirty-two male rats were randomly divided into four equal groups as follows: control, finasteride (30 mg/kg 14 days by gastric gavage), diabetes, and diabetes+finasteride. Malondialdehyde (MDA), superoxide dismutase (SOD), and total antioxidant status (TAS) levels in liver, kidney, and testis tissues, and nitric oxide (NO), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) levels in blood samples were examined. In addition, tissue sections were evaluated immunohistochemically (B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax)) and histopathologically. Induction of diabetes with streptozotocin resulted in an increase MDA, NO, IL-6, TNF-α levels whereas TAS and SOD decreased compared to the control group. Diabetes+Finasteride group was compared with the diabetes group decrease in MDA, NO, IL-6, TNF-α levels, and increase in TAS and SOD levels were observed. Finasteride suppressed apoptosis through the down regulation of Bax and the induction of the expression of Bcl-2 in the liver and kidney. Finasteride administration ameliorated some histopathological changes and decreased oxidative stress, apoptosis, and inflammation while increasing the antioxidant defense system in the STZ-induced diabetes group. In conclusion, finasteride might show a protective effect by suppressing oxidative stress and apoptosis and downregulation of proinflammatory cytokines in diabetic rats with its antioxidant and antiapoptotic effects. Human trials are needed before clinical application.