Effect Of Capsaicin On LPS-induced Macrophage Activation,Phagocytosis And Cytokine Production

ObjectiveIn order to investigate the anti-inflammatory activity of capsaicin,LPS was used to treat mouse peritoneal macrophages to establish a cell inflammatory model,and the anti-inflammatory activity of capsaicin was studied in vitro,which provided a scientific experimental basis for the development and utilization of capsaicin.MethodsIn this experiment,lipopolysaccharide-induced peritoneal macrophage inflammation model was established in vitro.MTT assay was used to detect the effects of capsaicin monotherapy group,lipopolysaccharide(LPS)and capsaicin compound group on the phagocytosis of mouse peritoneal macrophages.The effects of capsaicin monotherapy group,LPS and capsaicin compound group on the secretion of peritoneal macrophage cytokines IL-6 and TNF-? and NO production in inflammatory media were detected by ELISA.The results were detected by Real-time PCR.Effects of capsaicin monotherapy group,LPS and capsaicin compound group on the expression of macrophage cytokines IL-6,TNF-? and i NOS m RNA in peritoneal cavity of mice.ResultsThe OD values of macrophages in capsaicin monotherapy group,LPS and capsaicin compound group were higher than those in the control group.The difference was extremely significant(P<0.01),indicating that capsaicin monotherapy group,LPS and capsaicin compound group can increase the function of mouse peritoneal macrophages to phagocytose Staphylococcus aureus was enhanced,but the phagocytosis of mouse peritoneal macrophages by LPS and capsaicin compound group was lower than that of the monotherapy group.The capsaicin monotherapy group stimulated mouse peritoneal macrophages.Secretion of cytokines IL-6 and TNF-? in various concentrations of capsaicin and inflammatory mediator NO production were significantly higher than those in the control group(P<0.01).Capsaicin can enhance the secretion of peritoneal macrophage cytokines IL-6 and TNF-? and the production of inflammatory mediator NO;LPS and capsaicin compound group stimulate mouse peritoneal macrophages,and each concentration group of the composite drug group can inhibit LPS-induced secretion of peritoneal macrophage factors IL-6,TNF-? and inflammatory mediators of NO production,and with the increase in capsaicin concentration,inhibition increased,there is a clear dose-effect relationship(P<0.05,P<0.01),indicating that capsaicin can inhibit LPS-induced peritoneal macrophage cytokines IL-6,TNF-? secretion and inflammatory mediators NO production.The capsaicin monotherapy group stimulated mouse peritoneal macrophages,and the expression levels of cytokines IL-6,TNF-?,and i NOS in capsaicin concentrations increased significantly,compared with the control group.The difference was significant(P<0.01,P<0.05);LPS and capsaicin compound group stimulated mouse peritoneal macrophages to reduce the m RNA expression of IL-6,TNF-? and i NOS,and with the increase of capsaicin,IL-6,TNF-? and i NOS m RNA The expression of Caspase-3 was significantly decreased,and it was concentration-dependent;LPS and capsaicin compound group had significant difference compared with LPS group(P<0.01,P<0.05),indicating that capsaicin can inhibit LPS-induced mouse peritoneal macrophage IL-6,TNF-? and i NOS m RNA expression.ConclusionIn the concentration range of 25~100?g/m L,Capsaicin monotherapy group,LPS and capsaicin compound group all increased the ability of peritoneal macrophages of mice to phagocytose Staphylococcus aureus.When the capsaicin monotherapy group stimulated mouse peritoneal macrophages,it could induce the secretion of macrophage factors IL-6 and TNF-? in the peritoneal cavity of mice and the production of NO in inflammatory mediators;capsaicin could inhibit the LPS-induced mouse peritoneal cavity and the expression of IL-6,TNF-? and i NOS m RNA in macrophages.Capsaicin can increase the anti-inflammatory activity of mouse peritoneal macrophages.Anti-inflammatory effects may be achieved by increasing the secretion of cytokines IL-6 and TNF-? and inhibiting NO production pathways in inflammatory mediators.