Abstract
Background: Leydig cells secrete the steroid hormone, testosterone, which is essential for male fertility and reproductive health. Stress increases the secretion of glucocorticoid [corticosterone, (CORT) in rats] that decreases circulating testosterone levels in part through a direct action on its receptors in Leydig cells. Intratesticular CORT level is dependent on oxidative inactivation of CORT by 11β-hydroxysteroid dehydrogenase 1 (HSD11B1) in rat Leydig cells. Pain may cause the stress, thus affecting testosterone production in Leydig cells.Methods: Adult male Sprague–Dawley rats orally received vehicle control or 5 or 10 mg/kg dehydroepiandrosterone (DHEA) 0.5 h before being subjected to pain stimulation for 1, 3, and 6 h. In the present study, we investigated the time-course changes of steroidogenic gene expression levels after acute pain-induced stress in rats and the possible mechanism of DHEA that prevented it. Plasma CORT, luteinizing hormone (LH), and testosterone (T) levels were measured, and Leydig cell gene expression levels were determined. The direct regulation of HSD11B1 catalytic direction by DHEA was detected in purified rat Leydig, liver, and rat Hsd11b1-transfected COS1 cells.Results: Plasma CORT levels were significantly increased at hour 1, 3, and 6 during the pain stimulation, while plasma T levels were significantly decreased starting at hour 3 and 6. Pain-induced stress also decreased Star, Hsd3b1, and Cyp17a1 expression levels at hour 3. When 5 and 10 mg/kg DHEA were orally administered to rats 0.5 h before starting pain stimulation, DHEA prevented pain-mediated decrease in plasma T levels and the expression of Star, Hsd3b1, and Cyp17a1 without affecting plasma CORT levels. DHEA was found to modulate HSD11B1 activities by increasing its oxidative activity and decreasing its reductive activity, thus decreasing the intracellular CORT levels in Leydig cells.Conclusion: Stress induced by acute pain can inhibit Leydig cell T production by upregulation of corticosterone. DHEA can prevent the negative effects of excessive corticosterone by modulating HSD11B1 activity.
Highlights
Many stressors, such as noise, pain, diseases, and pollution, are present in our daily life (Munck et al, 1984; Chrousos and Gold, 1992; de Quervain et al, 2017)
The concentrations of plasma CORT in the control group were 36.96 ± 4.70, 39.66 ± 5.49, and 36.81 ± 6.78 ng/ml at hour 1, 3, and 6 during the course of pain stimulation, respectively, and there were no differences between these groups (Figure 1A)
During the course of pain stimulation, plasma CORT levels in pain-stimulated groups were significantly elevated at hour 1, 3, and 6, when compared to those from the control rats (Figure 1A), indicating that these rats were under stress condition starting at hour 1
Summary
Many stressors, such as noise, pain, diseases, and pollution, are present in our daily life (Munck et al, 1984; Chrousos and Gold, 1992; de Quervain et al, 2017). Stress induced the elevation of circulating glucocorticoid (GC) level (Munck et al, 1984; Chrousos and Gold, 1992). GCs directly inhibited T production by Leydig cells, which are responsible for 95% of plasma T levels in males (Hales and Payne, 1989; Monder et al, 1994b; Orr et al, 1994). Stress increases the secretion of glucocorticoid [corticosterone, (CORT) in rats] that decreases circulating testosterone levels in part through a direct action on its receptors in Leydig cells. Pain may cause the stress, affecting testosterone production in Leydig cells
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