Nuciferine protects against lipopolysaccharide-induced endometritis via inhibiting ferroptosis and modulating AMPKα/mTOR/HIF-1α signaling axis

Int Immunopharmacol. 2023 Nov;124(Pt B):110914. doi: 10.1016/j.intimp.2023.110914. Epub 2023 Sep 19.

Abstract

Nuciferine (NF) is an alkaloid isolated from Nelumbo nucifera and has been reported to exhibit a wide range of pharmacological effects. However, whether NF treatment exhibits a protective effect in endometritis remains unclear. Here, the protective effects of NF on lipopolysaccharide (LPS)-induced endometritis in mice were investigated in our research. The results showed that NF significantly reversed the uterine histopathological changes, inflammatory factor levels and myeloperoxidase (MPO) activity caused by LPS. Furthermore, we found that NF administration improved the reproductive capacity of mice with endometritis. Mechanistically, the expression of MyD88/nuclear factor-kappa B (NF-κB) and MAPK-related proteins in uterine tissue were decreased by NF treatment. Moreover, we observed the occurrence of ferroptosis in the LPS-induced endometritis mouse model, which was noticeably inhibited by NF treatment. In addition, we showed that NF exhibited anti-endometritis activity by modulating AMPKα/mTOR/HIF1α signaling axis. Finally, the molecular mechanism of the NF anti-inflammatory effect was clarified in mouse endometrial epithelial cells (mEECs). NF inhibited the releases of pro-inflammatory factors in LPS-induced mEECs via inhibiting NF-κB signaling pathway. All these findings suggest that NF may ameliorate LPS-induced endometritis caused by LPS, the mechanism of action is related to the ferroptosis, MyD88/NF-κB, MAPK and AMPKα/mTOR/HIF1α signaling pathway.

Keywords: AMPKα/mTOR/HIF-1α signaling axis; Ferroptosis; Lipopolysaccharide-induced endometritis; Nuciferine.

MeSH terms

  • Animals
  • Endometritis* / chemically induced
  • Endometritis* / drug therapy
  • Endometritis* / metabolism
  • Female
  • Ferroptosis*
  • Humans
  • Lipopolysaccharides / pharmacology
  • Mice
  • Myeloid Differentiation Factor 88 / metabolism
  • NF-kappa B / metabolism
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • NF-kappa B
  • Lipopolysaccharides
  • nuciferine
  • Myeloid Differentiation Factor 88
  • TOR Serine-Threonine Kinases