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Human placental mesenchymal stem cells regulate inflammation via the NF­κB signaling pathway.
Liu, Youyi; Zhang, Xiading; Hu, Yiwei; Kang, Mingzhu; Wu, Yibo; Wang, Yuan; Deng, Chao.
Afiliação
  • Liu Y; Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, P.R. China.
  • Zhang X; Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, P.R. China.
  • Hu Y; Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, P.R. China.
  • Kang M; School of Pharmaceutical Science, Jiangnan University, Wuxi, Jiangsu 214122, P.R. China.
  • Wu Y; Department of Obstetrics and Gynecology, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu 214062, P.R. China.
  • Wang Y; Department of Obstetrics and Gynecology, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu 214062, P.R. China.
  • Deng C; Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, P.R. China.
Exp Ther Med ; 24(5): 654, 2022 Nov.
Article em En | MEDLINE | ID: mdl-36168408
ABSTRACT
Emerging evidence has indicated that mesenchymal stem cells (MSCs) are involved in the modulation of inflammation. Human placenta-derived (HPL)-MSCs exist in sufficient quantities and play a role in immune regulation. However, the exact roles of HPL-MSCs in inflammation and the specific underlying mechanisms are not well defined. In the present study, HPL-MSCs were obtained from human fetal placentas, and further purified using a commercial kit. Using ELISA, reverse transcription-quantitative PCR, western blot, NO detection and other assays, the present study revealed that HPL-MSCs may improve lipopolysaccharide-induced macrophage inflammation by regulating macrophage polarization. Further mechanistic studies demonstrated that HPL-MSCs attenuated the NF-κB signaling pathway by regulating the expression of toll-like receptor 4 and the phosphorylation of IκBα and p65, which resulted in a reduction in the levels of inflammation. The present study indicated that HPL-MSCs may act as a novel target for the treatment of inflammation-related diseases.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article