Objective    To evaluate the effects of recombinant human neuregulin-1β on a rat model of adriamycin-induced dilated cardiomyopathy (ADR-DCM).     Methods    Matched adult male Sprague-Dawley rats were administered with 2.5 mg/kg adriamycin intravenously once a week for 10 weeks to establish models of ADR-DC

M. The ADR-DCM rats were randomly divided into 3 groups as follows: the rhNRG-1β group (rhNRG-1β

20  μg/kg

i.v.

once a day for 10 d

n=8)

the negative control group (excipient

n=8)

and the positive control group (digoxin

0.062 5 mg/kg

i.v.

once a day for 10 d

n=7). Another 8 normal SD rats in the same situation served as normal control group (control

n=8). Their heart function and hemodynamics were evaluate after the treatment. The ratio of heart weight/body weight was calculated and the thickness of LV parietes was measured. The pathological lesions of cardiac muscle tissues were evaluated after HE staining. Brain contents of natriuretic peptide (BNP) and troponin T (TnT) were determined. The animal treatment was all accorded to the ethical standards.     Results    Compare with the normal control group

the LVESD and LVEDD of ADR-DCM rats were increased (P0.01)

but the LVEF and LVFS were decreased (P0.01); the LVSP and  dp/dt

max

of ADR-DCM rats were decreased (P0.01) but the LVEDP was increased (P0.01). ADR-DCM rats had a decreased thickness of LV parietes (P0.05)

damaged cardiac muscle tissues and higher pathological lesions score (P0.05)

with increased plasma concentrations of BNP and TnT (P0.05). Compare with the control groups

rhNRG-1 treatment increased the LVSP and  dp/dt

max

(P0.05)

decreased LVEDP (P0.05) and the pathological lesions score (P0.05)

and had less damaged cardiac muscle tissues and decreased plasma concentrations of BNP and TnT (P0.05).     Conclusion    rhNRG-1 attenuates left ventricular damage and heart failure in a rat model of ADR-DCM.