2. Academic Validation
  3. Moracin M inhibits lipopolysaccharide-induced inflammatory responses in nucleus pulposus cells via regulating PI3K/Akt/mTOR phosphorylation

Moracin M inhibits lipopolysaccharide-induced inflammatory responses in nucleus pulposus cells via regulating PI3K/Akt/mTOR phosphorylation

  • Int Immunopharmacol. 2018 May:58:80-86. doi: 10.1016/j.intimp.2018.03.015.
Fang Guo 1,  Yong Zou 2,  Yongjiang Zheng 3
Affiliations

Affiliations

  • 1 Department of Obstetrics & Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
  • 2 Department of Blood Transfusion, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
  • 3 Department of Hematology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, China. Electronic address: [email protected].
PMID: 29558663 DOI: 10.1016/j.intimp.2018.03.015
Abstract

Moracin M, a phenolic component obtained from Mori Cortex, has been reported to have anti-inflammatory activities. The present study was designed to investigate the effects and mechanisms of Moracin M on lipopolysaccharide (LPS)-treated nucleus pulposus cells (NPCs) in intervertebral disc. NPCs were treated with moracin M at different concentrations for 1 h and then stimulated with LPS (0.5 μg/mL) for 24 h. The result demonstrated that moracin M could significantly inhibit LPS-induced inflammation. The elevated levels of IL-1β, TNF-α and IL-6 induced by LPS could be reversed by moracin M in NPCs. Moreover, moracin M increased the expressions of autophagy-related proteins and up-regulated the phosphorylation of PI3K/Akt/mTOR in LPS-treated NPCs. In conclusion, our data demonstrated that moracin M might inhibit LPS-induced PI3K and Akt phosphorylation, which leading to promote the Autophagy and inhibit the inflammatory mediator production in NPCs.

Keywords

Intervertebral disc degeneration; LPS; Moracin M; PI3K/Akt/mTOR phosphorylation.

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