The Anti-inflammatory Activities And Mechanism Of Coumarin From Durian And Triterpenoid From Chinese Acorns

Aim:We have previously studied the chemical constituents of durian and Chinese oak.Propacin is a coumarins isolated from durian and Q43 is a triterpenoid from Chinese oak.To explore the anti-inflammation effects of propacin and Q43,we investigate the effects and mechanisms of propacin and Q43 in LPS-induced cells models in vitro.Methods:In this paper,qRT-PCR,ELISA,Fluorescence microscopy and western blot were used to detect the release of inflammatory kinase,the expression of pro-inflammatory mediator and signal pathway,to investigate the anti-inflammatory activities and mechanisms of propacin and Q43.Result:Propacin suppressed the nitric oxide（NO）and prostaglandin E2（PGE₂）production in lipopolysaccharide（LPS）-stimulated macrophages without cytotoxicity.Propacin deceased the inducible nitric oxide synthase（iNOS）and cyclooxygenase-2（COX-2）expression on mRNA and protein level,downregulated interleukin-1β（IL-1β）,IL-6 and tumor necrosis factor-α（TNF-α）mRNA expression as well as the secretions of IL-6 and TNF-α.According to Western blot analysis,propacin deceased the phosphorylation of nuclear factor-kappa B（NF-κB）,inhibitor ofκB（IκBα）and mitogen-activated protein kinases（MAPKs）,suppressed nuclear translocation of NF-κB.Q43 inhibited NO and PGE₂ releasing in LPS-induced BV2 cells,suppressed i NOS and COX-2 expression on mRNA and protein levels.In addition,Q43decreased the mRNA levels of IL-1β,IL-6 and TNF-α,as well as the production of IL-6 and TNF-α.According to Western blot analysis,Q43 down-regulated the expression of p-NF-κB and p-IκBα,inhibited NF-κB nuclear translocation,inhibited phosphorylation of MAPKs proteins.Conclusion:Through suppress MAPK and NF-κB pathway,propacin inhibits inflammatory response mediated by abnormal macrophage activation,Q43inhibits neuroinflammatory response mediated by abnormal microglia activation.Therefore,propacin and Q43 may provide a potential therapeutic strategy for the treatment of inflammation.