Anti-inflammatory Effect and Mechanismof Chrysanthemum Indicum Decoction on RAW264.7 Inflammatory Cell Model
10.3870/j.issn.1004-0781.2024.08.003
- VernacularTitle:野菊花水提物对RAW264.7炎症细胞模型的抗炎作用及其机制
- Author:
Xin XIONG
1
;
Chuanqi HUANG
;
Lu CHENG
Author Information
1. 武汉市第一医院药学部,武汉 430022
- Keywords:
Chrysanthemum indicum;
Anti-inflammation effect;
RAW 264.7 inclammatory cell model;
Lipopoly-saccharide;
Nuclear factor-kappa B
- From:
Herald of Medicine
2024;43(8):1192-1198
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the anti-inflammatory effect and molecular mechanism of Chrysanthemum indicum decoction(C.indicum decoction,CID)through NF-κB signaling pathway based on RAW264.7 macrophages model induced by lipopolysaccharide(LPS).Methods MTT was used to select the appropriate concentration of CID on the activity of RAW 264.7 macrophages;Griess method and enzyme-linked immunosorbent assay(ELISA)were used to measure the release of nitric oxide(NO),tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in cells treated with 50,100 and 200 μg·mL-1 CID,respectively;and the relative contents expression levels of cyclooxygenase-2(COX-2)and inducible nitric oxide synthase(iNOS)in each group were analyzed by real-time fluorescent quantitative polymerase chain reaction(Real-time PCR);the relative production of nuclear factor-kappa B p65(NF-κB p65),inhibitor kappa B(IκB-α)and phosphorylated IκB-α(p-IκB-α)in each group was observed by Western blotting(WB).Results 50-200 μg·mL-1 CID significantly decreased the relative production of NO,TNF-α,and IL-6 in RAW264.7 macrophages induced by LPS(P<0.01),down-regulated the expression of COX-2 and iNOX mRNA(P<0.01),down-regulated the relative contents of p-IκB-α,total NF-κB p65 and nuclear NF-κB p65(P<0.01),and up-regulated the relative contents of IκB-α and cytoplasmic NF-κB p65(P<0.01).Conclusion CID could effectively inhibit the release of inflammatory factors from RAW 264.7 macrophages induced by LPS,and the mechanism may be related to the inhibition of inflammation by reducing the expression of TNF-α and other key proteins and regulating the inflammatory signaling pathway such as NF-κB.
