Dexamethasone-Induced Chronic Stress Decreases Biochemical Fluid Components and Seminal Vesicle Secreting Protein 4 Expression Via Epithelial Cell Apoptosis

Abstract

Background: Dexamethasone (DEX) has recently been used to treat inflammation and to induce the chronic stress (CS) in animal models. Although its adverse effects on testicular damage and seminal plasma reduction were previously reported, the changes in the seminal vesicle are still unexplored. This study aimed to investigate the effects of DEX on biochemical alterations in seminal vesicle fluid (SVF) and seminal vesicle tissue (SVT).

Methods: Male rats were divided into control and DEX groups (n = 20). CS animals were induced with DEX at 1.5 mg/KgBW for 21 consecutive days. CS behaviors were confirmed by the tests of tail suspension, forced swimming, and sucrose preference. Hormones and biochemical components in serum and SVF were evaluated. SVF volume and histomorphometry of SVT were observed. Expressions of apoptotic markers and seminal vesicle secreting protein 4 (SVS4) were determined.

Results: The results showed the reductions of seminal vesicle size and SVF volume in DEX rats. DEX increased the malondialdehyde (MDA) level in SVF, and DNA fragmentation revealed by the TUNEL assay. Serum testosterone and levels of magnesium and fructosamine in SVF of the DEX group were significantly decreased. DEX altered the thickness of the seminal vesicle wall. The expression of SVS4 was decreased in SVT induced with DEX. However, no difference in apoptotic expressions (Hsp70, procaspase-3, and procaspase-9) was observed between groups.

Conclusion: The DEX-induced CS caused the seminal vesicle changes, which were associated with DNA fragmentation. Decreases of fructosamine and SVS4 may be a cause of low-sperm quality such as motility and capacitation in CS men.