The influence of resveratrol on macrophage polarization and myocardial inflammatory injury in rats with experimental autoimmune myocarditis
Objective:To explore the effects of resveratrol on myocardial macrophage polarization and inflammatory in-jury in experimental autoimmune myocarditis(EAM)rats.Methods:Experimental myocarditis model was established and randomly divided into 3 groups:Control group(Control),EAM model group(EAM)and Resveratrol treatment group(Res-veatrol).The degree of macrophage infiltration were detected by immunofluorescence and the degree of myocardial injury was detected by HE stain.The expression of markers(iNOS and Arg1)of M1 and M2 macrophage and inflammatory factors were detected by Realtime PCR.Western blot was used to detect the expression changes of NLRP3 inflammasome protein components.Results:Large numbers of macrophages were observed infiltrating the myocardial tissue of EAM group rats,ac-companied by significant myocardial fiber rupture and dissolution;The mRNA expression of IL-6,IL-1β,TNF-α,and iNOS were significantly increased in the control group compared to the control group(P＜0.05,P＜0.05,P＜0.01,P＜0.01),The expression of Arg1 was significantly reduced compared to the control group(P＜0.05),and the difference was statisti-cally significant;Resveratrol can reduce the infiltration of macrophages and myocardial pathological injury score in EAM rats'myocardial tissue(P＜0.05),decrease the expression of IL-6,IL-1β,TNF-α,iNOS mRNA(P＜0.05),and increase the expression of Arg1(P＜0.01),with statistical significance.Meanwhile,compared with the Control group,the protein ex-pression of NLRP3 and Caspase-p10,pro-Caspase-1,and IL-1 β in the myocardial tissue of EAM rats was significantly in-creased.Resveratrol significantly reduced the protein expression of NLRP3,Caspase-p10,pro-Caspase-1,and IL-1 β(all P＜0.05),and the difference was statistically significant.Conclusion:Macrophage infiltration and polarization towards M1 type are associated with myocardial injury in EAM rats;Res may alleviate EAM myocardial injury by inhibiting polarization of M1 mac-rophages towards M2,activation of NLRP3 inflammasomes,and reduced release of inflammatory factors.
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维普
