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Sevoflurane inhibited inflammatory response induced by TNF-α in human trophoblastic cells through p38MAPK signaling pathway
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-02-18 , DOI: 10.1080/10799893.2020.1726951
Li Mo 1 , Shuzhen Hong 2 , Yi Li 3 , Zurong Hu 1 , Baoyi Han 1 , Zaomei Wei 1 , Jie Jia 1
Affiliation  

Abstract Purpose: Excessive inflammatory response is one of the possible pathogenic mechanisms of preeclampsia (PE). It remains unclear whether sevoflurane has an anti-inflammatory effect in human trophoblastic cells, which are corresponding to the dysfunction of placentas in PE. This study probed into the regulatory function of sevoflurane toward HTR8/SVneo cells so as to find PE pathology and PE treatment. Materials and methods: HTR8/SVneo cells were treated with sevoflurane, TNF-α with different concentrations, sevoflurane plus 10 ng/mL TNF-α and SB203580 plus 10 ng/mL TNF-α. Cell counting kit-8 (CCK-8) assays were performed to detect cell viability, while enzyme linked immunoSorbent assay (ELISA) was used to measure IL-6, IL-8, GM-CSF and MCP-1 levels in HTR8/SVneo cells. Besides, relative mRNA expression levels of IL-6 and IL-8 were tested via quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), and p38 phosphorylation-related protein expressions were assessed through western blot. Results: Cell viability remained stable when HTR8/SVneo cells were treated with or without sevoflurane and SB203580 in inflammatory microenvironment created by TNF-α. MCP-1 and GM-CSF levels, as well as gene expressions of IL-6 and IL-8 in HTR8/SVneo cells were greatly increased by TNF-α (5, 10 and 20 ng/mL), but reversed by sevoflurane and SB203580. Simultaneously, TNF-α-induced phosphorylation of p38MAPK signaling pathway was inhibited by sevoflurane and SB203580. Conclusions: Sevoflurane inhibited inflammatory response induced by TNF-α in human trophoblastic cells HTR8/SVneo through suppressing the phosphorylation of p38MAPK signaling pathway.

中文翻译:

七氟烷通过p38MAPK信号通路抑制TNF-α诱导的人滋养细胞炎症反应

摘要 目的:过度炎症反应是先兆子痫(PE)的可能致病机制之一。目前尚不清楚七氟醚是否对人类滋养细胞具有抗炎作用,这与 PE 中胎盘的功能障碍相对应。本研究探讨了七氟醚对HTR8/SVneo细胞的调节作用,以期发现PE病理学和PE治疗方法。材料和方法:HTR8/SVneo 细胞用七氟醚、不同浓度的 TNF-α、七氟醚加 10 ng/mL TNF-α 和 SB203580 加 10 ng/mL TNF-α 处理。进行细胞计数试剂盒-8 (CCK-8) 测定以检测细胞活力,而酶联免疫吸附测定 (ELISA) 用于测定 HTR8/SVneo 中的 IL-6、IL-8、GM-CSF 和 MCP-1 水平细胞。除了,通过定量实时逆转录聚合酶链反应 (qRT-PCR) 测试 IL-6 和 IL-8 的相对 mRNA 表达水平,并通过蛋白质印迹评估 p38 磷酸化相关蛋白的表达。结果:在 TNF-α 产生的炎症微环境中,HTR8/SVneo 细胞用或不用七氟醚和 SB203580 处理时,细胞活力保持稳定。MCP-1 和 GM-CSF 水平,以及 HTR8/SVneo 细胞中 IL-6 和 IL-8 的基因表达被 TNF-α(5、10 和 20 ng/mL)大大增加,但被七氟醚和SB203580。同时,TNF-α 诱导的 p38MAPK 信号通路磷酸化被七氟醚和 SB203580 抑制。结论:
更新日期:2020-02-18
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