Molecular mechanism of apigenin on inhibition of LPS-induced inflammatory mediators in murine macrophages
10.3969/j.issn.1000-484X.2015.06.007
- VernacularTitle:芹菜素抑制脂多糖诱导小鼠巨噬细胞分泌炎症介质的分子机制
- Author:
Guang WU
;
Ping FU
;
Yusheng ZHOU
;
Runmei ZHOU
- Publication Type:Journal Article
- Keywords:
Apigenin;
Heme oxygenase-1;
Murine macrophages
- From:
Chinese Journal of Immunology
2015;(6):753-757
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect and the mechanism of Apigenin on lipopolysaccharides ( LPS )-induced inflammatory mediators production in murine macrophages. Methods:The murine macrophage cell line RAW 264. 7 cells were cultured in vitro,and were treated with different concentration of Apigenin followed by LPS administration. Expression of heme oxygenase-1 ( HO-1),cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS),phosphorylation of p38 and IκB,nuclear translocation of Nrf2 were detected by Western blot. Production of Nitrite and nitrate ( NOx) was analyzed by colorimetric technique. Secretion of prosta-glandin E2 (PGE2) was detected by ELISA. Activation of NF-κB was measured by luciferase assay. Results: Western blot indicated that apigenin could induce RAW 264. 7 cells expression of HO-1, and pretreatment of SB203580, an inhibitor of p38 significantly inhibited apigenin induced HO-1 expression. In addition,Apigenin could also decrease the content of nuclear transcription factor Nrf2 in cytoplasm and increase its level in the nucleus. Silencing of Nrf2 by specific siRNA could inhibit apigenin-induced HO-1 expression. Furthermore,apigenin administration significantly inhibited LPS-induced NOx production and PGE2 secretion, COX-2 and iNOS expression,IκB phosphorylation and NF-κB activation,and transfection of HO-1 siRNA could reverse these actions. Conclusion:Apigenin inhibits LPS-induced inflammatory response through induction of HO-1 and inhibition of NF-κB in macrophages.
