p38MAPK/HSPB1 is involved in the regulatory effects of selenomethionine on the apoptosis, viability and testosterone secretion of sheep Leydig cells exposed to heat

Abstract

AbstractTestosterone derived from testicular Leydig cells (LCs) is important for male sheep, and the testis is susceptible to external temperature. The present study aimed to explore the alleviating effect of selenomethionine (Se‐Met) on heat‐induced injury in Hu sheep LCs. Isolated LCs were exposed to heat (41.5°C, heat exposure, HE) or not (37°C, nonheat exposure, NE), and cells in NE and HE were treated with 0 (C) or 8 μmol/L (S) Se‐Met for 6 h. Cell viability, testosterone level, and the expression of GPX1, HSD3B, apoptosis‐related genes and p38 mitogen‐activated protein kinase (p38MAPK)/heat shock protein beta‐1 (HSPB1) pathway were examined. The results showed that Se‐Met increased GPX1 expression (NE‐S vs. NE‐C: 2.28‐fold; HE‐S vs. HE‐C: 2.36‐fold, p < 0.05) and alleviated heat‐induced decrease in cell viability (HE‐S vs. HE‐C: 1.41‐fold; HE‐C vs. NE‐C: 0.61‐fold, p < 0.01), although the viability was still lower than that in the NE‐C cells (HE‐S vs. NE‐C: 0.85‐fold) and Se‐Met‐treated cells (HE‐S vs. NE‐S: 0.81‐fold). Se‐Met relieved heat‐induced decrease in testosterone level (HE‐S vs. HE‐C: 1.84‐fold, p < 0.05) and HSD3B expression (HE‐S vs. HE‐C: 1.67‐fold, p < 0.05). Se‐Met alleviated heat‐induced increase in Bcl2‐associated protein X (BAX) expression (HE‐C vs. HE‐S: 2.4‐fold, p < 0.05), and decrease in B‐cell lymphoma‐2 (BCL2) expression (HE‐S vs. HE‐C: 2.62‐fold, p < 0.05), resulting in increased BCL2/BAX ratio in the HE‐S cells (HE‐S vs. HE‐C: 5.24‐fold, p < 0.05). Furthermore, Se‐Met alleviated heat‐induced activation of p‐p38MAPK/p38MAPK (HE‐C vs. HE‐S: 1.79‐fold, p < 0.05) and p‐HSPB1/HSPB1 (HE‐C vs. HE‐S: 2.72‐fold, p < 0.05). In conclusion, p38MAPK/HSPB1 might be involved in Se‐Met‐mediated alleviation of heat‐induced cell apoptosis, cell viability and testosterone secretion impairments in sheep LCs.