| PartⅠThe effect of TNF-αexpression on ventricular arrhythmias in rats after myocardial infarctionObjective:To study the effect of TNF-αexpression on ventricular arrhythmias in rats with myocardial infarction.Methods : Sixty male Wistar rats were randomly divided into three groups: MI group( n=20),rhTNFR:Fc group( n=20) and Sham group( n=20). Rats with MI were established by liquid nitrogen cryoinjury method. Programmed electrical stimulation was imposed on the hearts to induce ventricular arrhythmia 30 days after myocardial infarction. Protein expression levels of TNF-αwere detected by Western blot and laser scanning confocal 30 days after myocardial infarction.Results:Compared with sham group, the protein expression levels of TNF-αwere significantly increased and the incidence of ventricular arrhythmias was significantly higher in MI group (P <0.05). Compared with MI group, the protein expression levels of TNF-αexpression significantly were reduced and the incidence of ventricular arrhythmias was also significantly lower in rhTNFR:Fc group (P <0.05).Conclusion:There is relationship between TNF-αexpression and ventricular arrhythmias after MI in rats. PartⅡThe role of TNF-αon regulation of Cx43 and ventricular arrhythmias after myocardial infarction in ratsObjective: To investigate the effect of TNF-αon regulation of Cx43 and ventricular arrhythmias in rats after myocardial infarction.Methods: Sixty male Wistar rats were randomly divided into three groups: MI group( n=20),rhTNFR:Fc group( n=20) and Sham group( n=20). Rats with MI were established by liquid nitrogen cryoinjury method. Programmed electrical stimulation was imposed on the hearts of the three groups to induce ventricular arrhythmia. Protein expression levels of TNF-αand Cx43 were detected by Western blot and the distribution of Cx43 was observed by laser scanning confocal on 30 days after myocardial infarction.Results:Compared with sham group, in MI group, the protein expression levels of TNF-αwere significantly increased(P<0.05); phoshporylated Cx43 protein levels were significantly decreased (P<0.05); nonphoshporylated Cx43 protein levels and the incidence of ventricular arrhythmias were higher (P<0.05). The location of Cx43 was distributed sparely at intercaleted disks in MI group. After MI rats were treated by rhTNFR:Fc, compared with MI group, the protein expression levels of TNF-αexpression significantly were reduced(P<0.05); phoshporylated Cx43 levels protein were higher and nonphoshporylated Cx43 levels were lower(P<0.05); the incidence of ventricular arrhythmias was decreased (P<0.05). In addtion, the abnormal distribution of Cx43 in rhTNFR:Fc group was reversed compared with MI group.Conclusion: Remodeling of Cx43 induced by TNF-αmay be an important role of ventricular arrhythmias in rats after myocardial infarction. |
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