CTRP9 overexpression attenuates palmitic acid-induced inflammation, apoptosis and impaired migration in HTR8/SVneo cells through AMPK/SREBP1c signaling.

Abstract

Obesity in pregnant mothers often leads to a range of obstetric complications, including miscarriage, pre-eclampsia, gestational hypertension and diabetes. C1q/TNF-related protein 9 (CTRP9) is an adipokine with an anti-inflammatory effect. The aim of the present study was to identify the role of CTRP9 in the pathogenesis of maternal obesity during pregnancy. Following treatment with palmitic acid (PA), HTR8/SVneo cell viability and CTRP9 expression were analyzed using Cell Counting Kit-8 (CCK-8), reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses. The effects of CTRP9 overexpression on cell viability, apoptosis, pro-inflammatory cytokine levels and migration were assessed using CCK-8, TUNEL, RT-qPCR and Transwell assays, respectively. Subsequently, sterol-regulatory element binding protein 1c (SREBP1c) overexpression efficiency was verified using RT-qPCR, and its effects on cell viability, apoptosis, pro-inflammatory cytokines and migration damage were then examined in HTR8/SVneo cells. The results showed that CTRP9 overexpression attenuated the inhibition of cell viability and apoptosis caused by PA in HTR8/SVneo cells, reduced pro-inflammatory cytokine release, improved cell migration and regulated the protein expression level of AMP-activated protein kinase (AMPK)/SREBP1c signaling. In addition, CTRP9 inhibited SREBP1c expression through AMPK signaling, thereby attenuating the inflammation, apoptosis and inhibited migration caused by PA in HTR8/SVneo cells. In brief, CTRP9 protected against inflammation, apoptosis and migration defects in HTR8/SVneo cells exposed to PA treatment through AMPK/SREBP1c signaling, which suggested the potential role of CTRP9 in alleviating the toxicity of PA.