文献类型： 外文期刊
作者： Li, Xu 1 ; Xu, Gaoqing 1 ; Li, Zhiqiang 1 ; Liu, Hongyu 1 ; Ma, Xin 1 ; Yang, Lianyu 1 ; Zhang, Pengju 2 ; Zhao, Jing 1 ; Wa 1 ;
作者机构： 1.Jilin Agr Univ, Coll Anim Sci & Technol, Changchun 130118, Peoples R China
2.Jilin Acad Agr Sci, Branch Anim Husb, Gongzhuling 136100, Jilin, Peoples R China
关键词： GnIH; Apoptosis; Bovine; Granulosa cells; p38
期刊名称：LIFE SCIENCES （ 影响因子：5.037； 五年影响因子：4.689 ）
ISSN： 0024-3205
年卷期： 2021 年 270 卷
页码：
收录情况： SCI
摘要： Gonadotropin-inhibiting hormone (GnIH) inhibits the synthesis and release of gonadotropin by binding to its receptor. GnIH is involved in animal reproductive regulation, especially ovary function. It can regulate the proliferation, apoptosis and hormone secretion of follicular cells. However, the role and molecular mechanism of GnIH in bovine granulosa cell (bGC) apoptosis is unclear. Here, the effects of GnIH on proliferation, apoptosis, and mitochondrial function of bGCs were detected. A 10(-6) mol/mL concentration of GnIH inhibited bGC proliferation, promoted GC apoptosis, and damaged mitochondrial function. Additionally, GnIH significantly decreased the phosphorylation level of p38 (P < 0.01). To explore the role of the p38 signaling pathway in the process of GnIH-induced apoptosis in bGCs, an activator of p38 (U46619) was used to pretreat bGCs. U46619 pretreatment significantly alleviated GnIH damage to bGCs, including proliferation, apoptosis, and mitochondrial function. In conclusion, these results demonstrated that GnIH inhibited proliferation and promoted apoptosis of bGCs via the p38 signaling pathway.
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