Lipopolysaccharide stimulates bovine endometrium explants through toll?like receptor 4 signaling and PGE2 synthesis
Lipopolysaccharide stimulates bovine endometrium explants through toll?like receptor 4 signaling and PGE2 synthesis
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脂多糖通过 Toll 样受体 4 信号传导和 PGE2 合成刺激牛子宫内膜外植体
DOI:
10.1016/j.plefa.2021.102272
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发表时间:
2021-04-22
影响因子:
3
通讯作者:
Mao, Wei
中科院分区:
文献类型:
--
作者:
Deng, Yang;Liu, Bo;Mao, Wei
Bovine endometrium infection with gram-negative bacteria commonly causes uterine diseases. Previous studies indicate that prostaglandin E2 (PGE2) is an inflammatory mediator in bacterial endometritis. However, the mechanism underlying lipopolysaccharide (LPS)-induced inflammatory response regulation in bovine endometrial explants remains elusive. In the present study, bovine explants were pre-treated with 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors before LPS stimulation. PGE2 secretion, prostaglandin synthetase, proinflammatory factor, damage-associated molecular pattern (DAMP), and related signaling pathway factor levels were evaluated. Using 15-PGDH inhibitors pre-treatment, LPS-treated bovine endometrial explants exhibited augmentation of PGE2 and DAMP expression, and upregulation of various signaling pathway factors. Protein kinase A (PKA), extracellular-signal-regulated kinase, and c-Jun N-terminal kinase phosphorylation and degradation of nuclear transcription factor-?B (NF-?B) inhibitors were induced in the pre-treated endometrial explants. The mechanism underlying LPS-induced PGE2 accumulation acting as a pro-inflammatory mediator through tolllike receptor 4 signaling in bovine explants could involve the PKA, mitogen-activated protein kinase, and NF-?B pathways.