Objective: To study the effects of epicatechin on inflammatory cytokines in lipopolysaccharide (LPS)-induced macrophage model and its mechanism. Method: The in vitro inflammation model was established by stimulating RAW 264.7 cells with LPS (1 mg·L-1) for 24 h. The toxic effect of macrophages were detected by 3-(4

5-Dimethylthiazol-2-yl)-2

5-diphenyltetrazolium bromide (MTT) assay. The content of nitricoxide (NO) was assayed by Griess reagent.Enzyme linked immunosorbent assay(ELISA) were used to assay the content of inflammatory mediators

such as tumor necrosis factor-α (TNF-α)

interleukin-1(IL-1) and interleukin-6 (IL-6) in cell supernatant. The protein expressions of nitric oxide synthase (iNOS) and the related proteins of mitogen-activated protein kinase (MAPK) pathway were tested by Western blot. Result: The cell viability was not significantly affected by epicatechin at 100 μmol·L-1. Compared with control group

LPS could significantly induce RAW 264.7 cells to secrete inflammatory mediators

like NO

TNF-α

IL-1 and IL-6(P<0.01). Compared with model group

25-100 μmol·L-1of epicatechin in LPS-induced RAW 264.7 cells greatly inhibited the release of inflammatory mediators

such as NO

TNF-α

IL-1 and IL-6 (P<0.05

P<0.01)

and inhibit the expressions of iNOS

and the protein expression of p38MAPK

ERK1/2 and JNK in a dose dependent manner. Conclusion: Epicatechin can inhibit LPS-induced inflammatory response in RAW 264.7 cells

and its anti-inflammatory effect may be related to reduction of inflammatory cytokines

like NO

TNF-α

IL-1 and IL-6

inhibition of the gene expression of iNOS and phosphorylation of p38MAPK

ERK1/2 and JNK.