促炎细胞因子
MAPK/ERK通路
激酶
内分泌学
内科学
TLR4型
肿瘤坏死因子α
信号转导
生物
蛋白激酶A
蛋白激酶B
化学
炎症
细胞生物学
医学
作者
Junsheng Dong,Yang Qu,Jianji Li,Luying Cui,Yefan Wang,Jiaqi Lin,Heng Wang
标识
DOI:10.1016/j.intimp.2018.01.021
摘要
The bovine uterus is subject to infection after calving, which may lead to endometritis. Elevated cortisol levels have been observed in postpartum cattle. However, the role of cortisol in the inflammatory response of the uterus has not been reported. The aim of this study was to investigate the anti-inflammatory effects of cortisol on lipopolysaccharide (LPS)-induced primary bovine endometrial epithelial cells (BEECs). BEECs were treated with various concentrations of cortisol (5, 15 and 30 ng/mL) in the presence of LPS. The mRNA expression of TLR4 and proinflammatory cytokines was measured with qPCR. The activation of NF-κB and MAPK signalling pathways was detected with Western blotting and immunofluorescence. Cortisol induced the down-regulation of the mRNA expression of toll-like receptor 4 (TLR4) and proinflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8, tumour necrosis factor–α (TNF-α), cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS). Cortisol inhibited the activity of nuclear factor-κB (NF-κB) via blocking the phosphorylation and degradation of IκB. Cortisol suppressed the phosphorylation of mitogen-activated protein kinase (MAPK), including extracellular signal-regulated kinase (ERK1/2), p38MAPK and c-Jun N-terminal kinase/stress-activated protein kinase (JNK). These results demonstrated that cortisol may exert its anti-inflammatory actions by regulating NF-κB activation and MAPK phosphorylation.
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