Mechanism of β2-adrenergic receptor in viral myocarditis through β-arrestin/ERK1/2 pathway
Objective:To investigate the role of β2-adrenergic receptor(β2-AR)in myocardial injury in mice with viral myocarditis(VMC)through β-arrestin/extracellular regulated protein kinases(ERK1/2)pathway.Methods:Forty mice were randomly divided into control group,VMC group,β2-AR inhibition group and β-arrestin inhibition group,with 10 mice in each group.Tie index,ejection fraction(EF)and fractional shortening(FS)were measured by echocardiography.HE staining was used to detect the pathological structure of myocardial tissue.The level of myo-cardial apoptosis was detected by Tunel kit.The protein levels of β2-AR,β-arrestin and ERK1/2 in myocardial tissue were detected by immunofluorescence staining.Serum creatine kinase(CK)and aspartate aminotransferase(AST)levels were detected by ELISA kits.Results:Compared with the control group,the Tie index was increased,EF and FS were decreased in the VMC group(all P＜0.05),the structure of myocardial tissue was loose and disordered,the infiltration of inflammatory cells was abundant,the apoptosis of myocardial cells was increased,and the expression ofβ2-AR,β-arrestin and ERK1/2 in myocardial tissue was increased.The serum levels of CK and AST were increased(all P＜0.05).Compared with VMC group,the Tie index was significantly decreased,EF and FS were increased(all P＜0.05),the myocardial injury was improved,the apoptosis of myocardial cells was decreased,and the expression ofβ2-AR,β-arrestin and ERK1/2 was decreased in myocardial tissue of mice in β2-AR inhibition group(all P＜0.05).Compared with VMC group,the expression of β-arrestin and ERK1/2 in myocardial tissue and the contents of CK and AST in serum were decreased in β-arrestin inhibition group(all P＜0.05).Conclusion:Inhibition of β2-AR can improve cardiac dysfunction and myocardial injury in VMC mice by down-regulating β-arrestin/ERK1/2 pathway.
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