The protective effects of Crocin on testopathy in fat-fed and streptozotocin-treated diabetic rats: An experimental study.

BACKGROUND

Male hypogonadism is associated with type II diabetes mellitus due to testicular dysfunction. Medicinal plants have received considerable attention for the management of diabetes and its complications.

OBJECTIVE

The aim of present study was to evaluate the anti-diabetic and protective influence of Crocin on testopathy in diabetic rats.

MATERIALS AND METHODS

In this experimental study, type II of diabetes mellitus was induced by high-fat diet and low dose of streptozotocin. Male Wistar rats (8 weeks, 150-200 gr, 18 rats; = 6 per group) were divided into a control group (standard diet), diabetic group (streptozotocin+high-fat diet), and treatment group (High-fat diet+streptozotocin+Crocin at 20 mg/kg/day, i.p. for 60 days). After 60 days, animals were euthanized, testis and epididymis were dissected, and weights of testes and sperm count were analyzed. Hematoxylin-eosin-stained was done for histopathological examination. Blood samples were collected for the assessment of serum glucose and cholesterol.

RESULTS

High-fat diet and streptozotocin significantly increased the serum glucose and cholesterol levels as compared to the control group (p 0. 001). Moreover, there was a significant decrease in the weight of right (p= 0.008) and left testes (p 0. 001) and also the total sperm count (p= 0.023) in the diabetic group compared with the control group. Current results also identified that type II diabetes mellitus induced degeneration in the morphology of seminiferous tubules. Application of Crocin could significantly decrease serum glucose and cholesterol levels (p= 0.003). Furthermore, Crocin treatment significantly increased the weight of the right (p= 0.026) and left (p= 0.014) testes and total sperm count (p= 0.000). Also, Crocin could attenuate the pathological changes of the testes in the treatment group.

CONCLUSION

Present findings concluded that Crocin treatment improved diabetic testopathy and impairment of seminiferous tubules induced by high-fat diet and streptozotocin.