摘要
Objective To explore the role of coxsackievirus and adenovirus receptor（CAR） in cardiotoxicity infected by coxsackieviras B3. Methods A toxic cellular model was established in vitro by adding myocarditic coxsackievirus B3 （CVB3m） into the culture of neonatal mouse cardiomyocytes. 48 h later, the cardiomyocytes were divided into control, CVB3m, and CAR antibody ＋ CVB3m groups. CVB3m-mediated myocytopathic effect of above three groups was observed after further culturing for 48h. At the same time, the cardiomyocytes＇ viability of above three groups was assessed by MTT assay. Results The degree of cytopathic effect（CPE） of CAR antibody ＋ CVB3m group was significantly lower than CVB3m group （ P 〈 0. 01 ） and there was a significant increase in cell viability in CAR antibody ＋ CVB3m group compared with CVB3m group（ P 〈 0. 01 ）. No significant difference was found between CAR antibody ＋ CVB3m group and control group. Conclusion CAR antibody possesses a protective effect on CVB3m infected cardiomyoctyes, which indicates that CAR may play an important role in mediating cardiotoxicity infected by CVB3m.
Objective To explore the role of coxsackievirus and adenovirus receptor(CAR)in cardiotoxicity infected by coxsackievirus B3. Methods A toxic cellular model was established in vitro by adding myocarditic coxsackievirus B3(CVB3m)into the culture of neonatal mouse cardiomyocytes.48 h later, the cardiomyocytes were divided into control, CVB3m, and CAR antibody+CVB3m groups. CVB3m-mediated myocytopathic effect of above three groups was observed after further culturing for 48h. At the same time,the cardiomyocytes’viability of above three groups was assessed by MTT assay. Results The degree of cytopathic effect(CPE)of CAR antibody+CVB3m group was significantly lower than CVB3m group (P<0.01)and there was a significant increase in cell viability in CAR antibody+CVB3m group compared with CVB3m group(P<0.01). No significant difference was found between CAR antibody+CVB3m group and control group. Conclusion CAR antibody possesses a protective effect on CVB3m infected cardiomyoctyes, which indicates that CAR may play an important role in mediating cardiotoxicity infected by CVB3m.
