Correlation between PRDX2 and spermatogenesis under oxidative stress

Abstract

Background: Obesity is one of the world's diseases that endanger human health, causing systemic inflammation caused by excessive reactive oxygen damage. An increase in the proportion of obese people with reduced sperm motility has been reported. But the mechanism behind it remains unclear. Peroxiredoxin 2 (PRDX2) is a member of the peroxidase family that effectively removes hydrogen peroxide. This study is to clarify the expression of PRDX2 in the testes of obese mice and lay a foundation for further exploration of the regulatory and protective effects of PRDX2 on spermatogenesis.

Method: A model of high-fat-induced obesity in animals was constructed, and the expression of PRDX2 in the testes of the two groups was detected by immunohistochemistry, western blotting, immunofluorescence and other techniques. Hydrogen peroxide (H₂O₂) and cholesterol were co-cultured in testicular support cells for 48 h to observe the expression of PRDX2.

Result: PRDX2 expression was reduced in the testes of the obese group, and immunohistochemistry showed that it was mainly localized to supporting cells. H₂O₂ inhibits the expression of PRDX2 in Sertoli cells, and high cholesterol upregulates the expression of PRDX2 in Sertoli cells.

Conclusion: PRDX2 has some antioxidant properties against changes in the testicular environment caused by HFD. And under short-term oxidative stress to enhance its antioxidant capacity. PRDX2 may be involved in maintaining the oxidative balance of the spermatogenesis environment.

Keywords: Obesity; PRDX; Spermatogenesis; Testis.