Molecular mechanism of apigenin on inhibition of LPS-induced inflammatory mediators in murine macrophages / 中国免疫学杂志
Chinese Journal of Immunology
;
(12): 753-757, 2015.
Article
in Chinese
| WPRIM
| ID: wpr-468227
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Chinese Journal of Immunology
Year:
2015
Type:
Article
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