CTRP9 overexpression attenuates palmitic acid‑induced inflammation, apoptosis and impaired migration in HTR8/SVneo cells through AMPK/SREBP1c signaling
- Li Li
- Zhongyi Gu
- Junjie Zhang
Affiliations: Department of Obstetrics and Gynecology, Changhai Hospital, Naval Medical University, Shanghai 200433, P.R. China
- Published online on: May 20, 2022 https://doi.org/10.3892/etm.2022.11386
Copyright: © Li
et al. This is an open access article distributed under the
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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.