子宫内膜炎
PI3K/AKT/mTOR通路
安普克
NF-κB
脂多糖
MAPK/ERK通路
信号转导
髓过氧化物酶
NFKB1型
炎症
化学
药理学
生物
细胞生物学
内分泌学
内科学
蛋白激酶A
医学
磷酸化
生物化学
转录因子
基因
怀孕
遗传学
作者
Peng Jiang,Linxian Zhao,Hu R,Zanjing Zhai,Jian Guo,Kai Zhang
标识
DOI:10.1016/j.intimp.2023.110914
摘要
Nuciferine (NF) is an alkaloid isolated from Nelumbo nucifera and has been reported to exhibit a wide range of pharmacological effects. However, whether NF treatment exhibits a protective effect in endometritis remains unclear. Here, the protective effects of NF on lipopolysaccharide (LPS)-induced endometritis in mice were investigated in our research. The results showed that NF significantly reversed the uterine histopathological changes, inflammatory factor levels and myeloperoxidase (MPO) activity caused by LPS. Furthermore, we found that NF administration improved the reproductive capacity of mice with endometritis. Mechanistically, the expression of MyD88/nuclear factor-kappa B (NF-κB) and MAPK-related proteins in uterine tissue were decreased by NF treatment. Moreover, we observed the occurrence of ferroptosis in the LPS-induced endometritis mouse model, which was noticeably inhibited by NF treatment. In addition, we showed that NF exhibited anti-endometritis activity by modulating AMPKα/mTOR/HIF1α signaling axis. Finally, the molecular mechanism of the NF anti-inflammatory effect was clarified in mouse endometrial epithelial cells (mEECs). NF inhibited the releases of pro-inflammatory factors in LPS-induced mEECs via inhibiting NF-κB signaling pathway. All these findings suggest that NF may ameliorate LPS-induced endometritis caused by LPS, the mechanism of action is related to the ferroptosis, MyD88/NF-κB, MAPK and AMPKα/mTOR/HIF1α signaling pathway.
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