细胞凋亡
细胞生物学
生物
p38丝裂原活化蛋白激酶
受体
信号转导
内科学
内分泌学
卵巢
细胞生长
激素
MAPK/ERK通路
生物化学
医学
作者
Xu Li,Gaoqing Xu,Zhiqiang Li,Hongyu Liu,Xin Ma,Lianyu Yang,Pengju Zhang,Jing Zhao,Jun Wang,Wenfa Lu
出处
期刊:Life Sciences
[Elsevier BV]
日期:2021-01-17
卷期号:270: 119063-119063
被引量:8
标识
DOI:10.1016/j.lfs.2021.119063
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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