p38MAPK/HSPB1 参与硒代蛋氨酸对受热的绵羊 Leydig 细胞的凋亡、活力和睾酮分泌的调节作用。
p38MAPK/HSPB1 is involved in the regulatory effects of selenomethionine on the apoptosis, viability and testosterone secretion of sheep Leydig cells exposed to heat.
发表日期:2024 Sep
作者:
Yinying Xu, Yuting Xia, Jie Zhao, Hao Yu, Yanli Zhang, Dagan Mao
来源:
Cell Death & Disease
摘要:
来自睾丸间质细胞 (LC) 的睾酮对雄性绵羊很重要,而且睾丸对外部温度很敏感。本研究旨在探讨硒代蛋氨酸(Se-Met)对湖羊LCs热损伤的缓解作用。将分离的 LC 暴露于热(41.5°C,热暴露,HE)或不暴露(37°C,非热暴露,NE),并且 NE 和 HE 中的细胞用 0 (C) 或 8μmol/L (S) 处理Se-Met 6小时。检查细胞活力、睾酮水平以及 GPX1、HSD3B、凋亡相关基因和 p38 丝裂原激活蛋白激酶 (p38MAPK)/热休克蛋白 beta-1 (HSPB1) 通路的表达。结果显示,Se-Met 增加 GPX1 表达(NE-S 与 NE-C:2.28 倍;HE-S 与 HE-C:2.36 倍,p< 0.05),并减轻热诱导的细胞活力下降(HE-S vs. HE-C:1.41 倍;HE-C vs. NE-C:0.61 倍,p< 0.01),尽管活力仍低于 NE-C 细胞(HE-S与 NE-C:0.85 倍)和 Se-Met 处理的细胞(HE-S 与 NE-S:0.81 倍)。 Se-Met 可缓解热诱导的睾酮水平下降(HE-S 与 HE-C:1.84 倍,p< 0.05)和 HSD3B 表达下降(HE-S 与 HE-C:1.67 倍,p< 0.05) 。 Se-Met 缓解热诱导的 Bcl2 相关蛋白 X (BAX) 表达增加(HE-C 与 HE-S:2.4 倍,p< 0.05),以及 B 细胞淋巴瘤 2 (BCL2) 表达减少(HE-S vs. HE-C:2.62 倍,p< 0.05),导致 HE-S 细胞中 BCL2/BAX 比率增加(HE-S vs. HE-C:5.24 倍,p< 0.05) 。此外,Se-Met 还可减轻热诱导的 p-p38MAPK/p38MAPK(HE-C 与 HE-S:1.79 倍,p< 0.05)和 p-HSPB1/HSPB1(HE-C 与 HE-S: 2.72 倍,p< 0.05)。总之,p38MAPK/HSPB1 可能参与 Se-Met 介导的绵羊 LC 中热诱导细胞凋亡、细胞活力和睾酮分泌损伤的缓解。© 2024 Wiley periodicals LLC。
Testosterone 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.© 2024 Wiley Periodicals LLC.