Icariin protects testicular damage in streptozotocin-induced diabetic rats through regulation of glycolysis pathway

Abstract

Objective This study aims to investigate potential beneficial actions of icariin (ICA) on testicular spermatogenic function in male rats with streptozotocin (STZ)-induced diabetes and to explore the underlying mechanisms. Background: ICA was found to reduce blood glucose, regulate the endocrine function of the reproductive system, and improve testicular spermatogenic function. Methods Adult rats were intraperitoneally injected with STZ (65 mg/kg) to induce type 1 diabetes mellitus (T1DM). Diabetic rats were randomly classified intoT1DM ( n = 6) and T1DM + ICA ( n = 6) groups. Rats without STZ and ICA treatment were assigned as control group ( n = 6). The morphology of testicular tissues was examined by histological staining. The mRNA and protein expression levels were determined by quantitative real-time PCR, Western blot and immunostaining, respectively. Results Rats from T1DM group showed a reduction in epididymis and testis weight, and a decrease in sperm count when compared to control group ( p < 0.01), which was attenuated by ICA treatment ( p < 0.05) Diabetic rats from T1DM group also exhibited reduced diameter and area of seminiferous tubules, along with decreased spermatogonia and primary spermatocytes number when compared to control group ( p < 0.01), which was partially reversed by ICA treatment ( p < 0.05) Rats from T1DM group exhibited down-regulation of PCNA mRNA and protein in the testis when compared to control group ( p < 0.01); while ICA treatment up-regulated PCNA expression in the testis of diabetic rats compared to T1DM group ( p < 0.05). Rats from T1DM group showed up-regulation of Bax and capase-3 and down-regulation of Bcl-2, PKM2, HK2 and lactate dehydrogenase A in the testes when compared to control group ( p < 0.05), which was reversed by ICA treatment ( p < 0.05). Conclusion These findings suggest that ICA may exert its protective effects on testicular damage in diabetic rats through modulation of glycolysis pathway and suppression of apoptosis.