Icariin Protects Testicular Damage in Streptozotocin-induced Diabetic Rats Through Regulation of Glycolysis Pathway
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Pathology
Pharmacology
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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. 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 ( = 6) and T1DM + ICA ( = 6) groups. Rats without STZ and ICA treatment were assigned as control group ( = 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 ( < 0.01), which was attenuated by ICA treatment ( < 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 ( < 0.01), which was partially reversed by ICA treatment ( < 0.05) Rats from T1DM group exhibited down-regulation of PCNA mRNA and protein in the testis when compared to control group ( < 0.01); while ICA treatment up-regulated PCNA expression in the testis of diabetic rats compared to T1DM group ( < 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 ( < 0.05), which was reversed by ICA treatment ( < 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.