Wilforine inhibits LPS-induced inflammatory response in RAW264.7 cells by regulating the TLR4/MyD88/TRAF6 signaling pathway
10.12206/j.issn.2097-2024.202111068
- VernacularTitle:雷公藤次碱通过调控TLR4/MyD88/TRAF6信号通路抑制LPS诱导的RAW264.7细胞炎症反应
- Author:
Ying WANG
1
;
Minxin ZHANG
1
;
Bing LIN
2
Author Information
1. .
2. Department of Clinical Medicine, No. 900 Hospital of Joint Logistics Force of the PLA, Fuzhou 350025, China.
- Keywords:
Tripterygium wilfordii;
wilforine;
anti-inflammation;
TLR4;
MyD88;
NF-κB
- From:
Journal of Pharmaceutical Practice and Service
2022;40(6):505-509
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the anti-inflammatory effect and mechanism of wilforine. Methods Anti-inflammatory activity of wilforine was investigated in LPS-induced RAW264.7 cells. The cytokines production of RAW264.7 cells was analyzed by ELISA assay and the cell viability was assessed by CCK-8 method. The expression of TRAF6, the phosphorylation of IRAK, p38, ERK and JNK, the degradation of inhibitory κBα (IκBα) and the nuclear translocation of NF-κB p65 were further investigated by western blot. Results Triptolide had no significant toxicity to RAW264.7 cells at concentrations of 25, 50 and 100 μmol/L. and could significantly inhibit the contents of cytokines NO, IL-1β, TNF-α and IL-6. Wilforine significantly decreased the expression of TRAF6 and phosphorylation of IRAK, and inhibited the phosphorylation of ERK, p38, and JNK and degradation of IκBα, and reduced the level of nuclear translocation of NF-κB p65. Conclusion The anti-inflammatory activity of wilforine of LPS-induced RAW264.7 cells is probably via TLR4/MyD88/TRAF6 signaling pathway.
