Lipoxin A4 (LXA4) Improved LPS Induced Preeclampsia via Regulation Nrf2-ARE Signaling Pathway In Vitro

The aim is to discuss effects and mechanism of LXA4's improvement effect in LPS induced preeclampsia in vitro study. Using LPS induced HTR-8/SVneo to make preeclampsia cell model. Evaluating ROS, MDA, SOD and GSH in difference groups. It was measured cell proliferation, apoptosis, invasion and migration by CCK-8, flow cytometry, transwell and wound healing assay in difference groups. Relative proteins including Nrf2 and HO-1 were measured by WB assay. With LPS stimulating, ROS and MDA were significantly up-regulation and GSH and SOD levels were significantly depressed, meanwhile, cell proliferation was significantly downregulation with cell apoptosis significantly increasing, invasion cell number and wound healing rate were significantly depressed (p < 0.001, respectively) with Nrf2 and HO-1 proteins levels were significantly down-regulation (p < 0.001, respectively) in LPS groups. LXA4 supplement, cell biological activities were significantly up-regulation, however, after Nrf2 knockdown, the LXA4 treatment effects were disappear. LXA4 has effects to improve LPS induced preeclampsia to enhance cell biological activities by regulation Nrf2/HO-1 pathway in vitro study.

Automated summary

The aim of this study was to discuss the effects and mechanism of LXA4's improvement effect in LPS-induced preeclampsia in an in vitro study. LPS induction was used to create a preeclampsia cell model. Various parameters such as ROS, MDA, SOD, and GSH were evaluated in different groups. Cell proliferation, apoptosis, invasion, and migration were measured using assays such as CCK-8, flow cytometry, transwell, and wound healing assay. Protein levels of Nrf2 and HO-1 were measured using Western blot assay. Results showed that LPS stimulation led to up-regulation of ROS and MDA levels, down-regulation of GSH and SOD levels, and significant changes in cell biological activities. However, supplementation with LXA4 led to significant improvement in these activities, but these effects disappeared after Nrf2 knockdown. This study suggests that LXA4 can improve LPS-induced preeclampsia by regulating the Nrf2/HO-1 pathway in an in vitro setting.