LIU Qi-liang,SONG Yao-ming,LIU Chao.Neuregulin-1β inhibits cardiomyocyte apoptosis in adriamycin-induced rat cardiomyopathy by regulating bcl-2 and bax[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(24):2448-2451.
LIU Qi-liang,SONG Yao-ming,LIU Chao.Neuregulin-1β inhibits cardiomyocyte apoptosis in adriamycin-induced rat cardiomyopathy by regulating bcl-2 and bax[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(24):2448-2451.DOI:
Neuregulin-1β inhibits cardiomyocyte apoptosis in adriamycin-induced rat cardiomyopathy by regulating bcl-2 and bax
Objective To investigate the cardiomyocyte apoptosis and protein expressions of bcl-2 and bax in adriamycin (ADM)-induced myocardial damage in rats treated with neuregulin-1β (NRG-1β). Methods Sixty male SD rats weighing 200 to 250 g were randomly divided into 3 groups: control
ADR-DCM and ADR+NRG groups. ADR-DCM group (n=20) was weekly injected 2.0 mg/kg of ADR via tail vein once a week for 8 weeks to produce cardiomyopathy. The rats of ADR+NRG group (n=20) was given an injection of NRG-1β at 10 μg/(kg·d) via tail vein for 5 d after the establishment of cardiomyopathy by ADR injection. The animals from control group (n=20) received 2 ml/kg normal saline by injection
once a week for 8 weeks. Nine weeks later
rats were executed under anesthesia and their heart was resected. Apoptotic cardiomyocytes were detected by using the terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method. The expressions of bcl-2 and bax protein were determined by Western blotting. Results The index of apoptotic cardiomyocytes was increased significantly in ADR-DCM group and ADR+NRG group compared with control group (P0.05)
and compared with ADR-DCM group
the index of apoptotic cardiomyocytes was significantly lower in ADR+NRG group (P0.05); compared with ADR-DCM group
the expressions of bcl-2 protein was increased significantly (P0.05)
and the expression of bax protein was induced significantly decreased in ADR+NRG group (P0.05). Conclusion NRG-1β suppresses cardiomyocyte apoptosis induced by ADR by upregulating the expression of bcl-2 and downregulating the expression of bax.
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