The silencing of ApoC3 suppresses oxidative stress and inflammatory responses in placenta cells from mice with preeclampsia via inhibition of the NF-κB signaling pathway

ConclusionSilencing ApoC3 could suppress the NF-κB signaling pathway, thereby exercising a protective effect on cell injury induced by oxidative stress and reducing inflammatory responses.Graphical abstractThe molecular mechanism involving silenced APOC3 regulating the oxidative stress and inflammatory responses in placenta cells of preeclampsia mice via inhibition of the NF-κB signaling pathway. In preeclampsia mice, up-regulated APOC3 increased the expression of p65 and inhibited the expression of phosphorylation of IkBα, thus resulting in the oxidative stress injury and inflammatory responses of placenta cells. While silenced APOC3 could decrease the expression of hs-CPR, IL-6 and TNF-α and the level of MDA, 8-isoprostane and ox-LDL but increase the activity of MMP-2 and MMP-9, so that promoted the survival but inhibited the apoptosis of placenta cells, and then the oxidative stress injury was reduced and cell inflammation was reduced.
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research