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

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.

Keywords:

• Sevoflurane
• TNF-α
• trophoblast cells
• p38MAPK signaling pathway
• inflammatory response

Disclosure statement

No potential conflict of interest was reported by the author(s).

Availability of data and materials

The analyzed data sets generated during the study are available from the corresponding author on reasonable request.

Additional information

Funding

This work was supported by the Science Technology Department of Guangdong Province (Grant No. 2017A040405033).