Sevoflurane inhibited inflammatory response induced by TNF-α in human trophoblastic cells through p38MAPK signaling pathway.

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-alpha with different concentrations, sevoflurane plus 10 ng/mL TNF-alpha and SB203580 plus 10 ng/mL TNF-alpha. 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-alpha. 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-alpha (5, 10 and 20 ng/mL), but reversed by sevoflurane and SB203580. Simultaneously, TNF-alpha-induced phosphorylation of p38MAPK signaling pathway was inhibited by sevoflurane and SB203580. Conclusions: Sevoflurane inhibited inflammatory response induced by TNF-alpha in human trophoblastic cells HTR8/SVneo through suppressing the phosphorylation of p38MAPK signaling pathway.