Role of JNK, TGF-β1, Akt, IL-1β and INSL-3 in proanthocyanidin protection against apoptosis in diabetic rat testis

Abstract

ABSTRACT We investigated how proanthocyanidin treatment altered c-Jun N-terminal kinases, transforming growth factor beta 1, serine/threonine-specific protein kinase, interleukin 1 beta and insulin-like 3 expression in the testis of diabetic rats. We used 24 Wistar albino male rats divided into four groups. Group 1 was untreated control. Group 2 was treated with 40 mg/kg streptozotocin (STZ) for 5 days. Group 3 was treated with 40 mg/kg STZ + 250 mg/kg proanthocyanidin once daily for six weeks. Group 4 was treated with 40 mg/kg STZ + 250 mg/kg proanthocyanidin. Superoxide dismutase activity was reduced in groups 3 and 4 compared to group 2. Glutathione peroxidase activity was increased significantly in groups 3 and 4 compared to groups 1 and 2. Catalase activity was decreased in group 4 compared to group 2. We found that proanthocyanidin increased cell proliferation in diabetic testis. Phospho-JNK and TGF-β1 immunostaining was decreased groups 3 and 4 compared to group 2, while p-Akt immunostaining was increased in groups 3 and 4. The number of IL-1β immunostained cells in groups 3 and 4 was decreased compared to group 2. INSL-3 immunostaining was increased significantly in group 3 compared to group 2. Our findings indicate that proanthocyanidin ameliorated diabetes related testicular dysfunction. Proanthocyanidin contributes to a balanced oxidant-antioxidant status, and balanced proliferation and apoptosis activity in the germinal cells.