Regulation Mechanism Of Echinacea Purpurea Extract-cichoric Acid On TLR4 Signal Pathway In PBMC Of Yak

Chicoric acid(CA),as one of the important active constituents of Echinacea extract,has a wide range of pharmacological activities.At present,the research on the anti-inflammatory activity of CA is mainly in the aspects of tissues and organs,hematology analysis,There is no relevant study on whether it exerts an immunological anti-inflammatory effect through the cell signaling pathway.Lipopolysaccharide(LPS)is often used to establish an inflammatory model.The inflammatory response triggered by LPS is usually through activation of the Toll loke receptors 4(TLR4)signal transduction pathway and triggers other signaling pathways that ultimately induce some inflammatory factors.Based on the above principles,this study used yak as the research object,and established an in vitro inflammatory model with LPS.The effects of cichoric acid on the production and expression of some inflammatory factors in yak peripheral blood mononuclear cells were studied by ELISA and RT-PCR.At the same time,from the aspect of TLR4 signal transduction pathway,the anti-inflammatory mechanism of chicoric acid on the peripheral blood mononuclear cell(PBMC)of yak was investigated by RT-PCR and WB method.The main results are as follows: 1.The results of CA on inflammatory response LPS-induced PBMC of yak showed that compared with LPS treatment group,the contents and mRNA expression level of IL-6,IL-8,IL-1?,TNF-? and INF-?in PBMC of yak can be significantly reduced after the combination of CA and LPS(P<0.05),but the content and mRNA expression of IL-10 was significantly increase(P< 0.05).2.The results of CA on the TLR4 signaling pathway LPS-induced in PBMC of yak show that CA significantly inhibited the mRNA expression and protein levels of MyD88 and TRAF6 in LPS4-induced TLR4 signaling pathway,and significantly decreased the mRNA expression of NF-?B(P<0.05).In summary,CA can inhibit inflammatory response that LPS-induced in PBMC of yak,It is speculated that it maybe through MyD88-dependent of TLR4 signaling pathway to activates the TLR4/MyD88/TRAF6/NF-?B pathway and regulates the release and expression of inflammatory cytokines,thereby exerting an immunological anti-inflammatory effect.