课程组在热应激损伤睾丸功能的防治方面取得新进展

      近日，动科学院动物热应激疾病防治团队在微量元素研究的主流国际期刊Biological Trace Element Research发表题为“Zinc Protects against Heat Stress–Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in TM3 Leydig Cells”的研究论文，课程组负责人熊永洁博士为论文第一作者，贺绍君博士为通讯作者。

论文信息：Yongjie Xiong, Jing Li, Shaojun He. Zinc Protects against Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in TM3 Leydig Cells. Biol Trace Elem Res. 2021 Mar 18. doi: 10.1007/s12011-021-02673-7. Online ahead of print.

期刊分区：BIOCHEMISTRY & MOLECULAR BIOLOGY Q3, IF=3.738 (2020)

论文摘要：Heat stress (HS)-induced apoptosis in Leydig cells is mediated by various molecular mechanisms, including endoplasmic reticulum (ER) stress. Zinc, an inorganic mineral element, exhibits several cytoprotective properties, but its potential protective action against Leydig cell apoptosis and the related molecular mechanisms has not been fully elucidated. In this study, we evaluated the effects of zinc sulfate, a predominant chemical form of zinc, exerted on cell viability, apoptosis, and testosterone production in HS-treated TM3 Leydig cells and investigated the underlying signaling pathways. HS treatment inhibited cell viability and induced apoptosis, which was accompanied by the induction of the activity of caspase 3, an executioner of apoptosis, involved in the expression of pro-apoptotic protein B cell lymphoma 2-associated X protein (Bax), and in the reduction of the expression of anti-apoptotic protein B cell lymphoma 2 (Bcl-2), thereby activating ER stress marker protein expression (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP)). However, zinc sulfate led to the attenuation of deleterious effects, including increases in apoptosis, caspase-3 activity, Bax, GRP78, and CHOP expression, and decreases in cell viability and Bcl-2 protein expression in cells treated with HS or thapsigargin (an ER stress activator). Furthermore, 4-phenylbutyric acid (an ER stress inhibitor) treatment markedly alleviated the HS-induced adverse effects in cells exposed to HS, which was similar to zinc sulfate. Additionally, zinc sulfate supplementation in the culture medium effectively restored the HS-induced decrease in testosterone levels in HS-treated cells. In summary, these findings indicate that HS triggers apoptosis in TM3 Leydig cells via the ER stress pathway and that zinc confers protection against these detrimental effects. This study provides new insights into the benefits of using zinc against HS-induced apoptosis and cell injury.