Objective To observe the influence of β₃-AR antagonist on expression of Suppressor of cytokine signalling 3 (SOCS3), receptor serine/threonine kinases (Akt), pAkt and Caspase3 in heart failure (HF) model rats induced by isoprenaline (ISO), observe the influence of β₃-AR antagonist in HF, and provide a theoretical basis for prevention and control HF.

Methods (1) The rats were randomly divided into three groups:Igroup (10 weight-matched normal adult rats as controls), IIgroup (25 rats with ISO induced heart failure) and IIIgroup (25 rats with ISO induced heart failure but received SR59230A treatment). (2) Echocardiography examinated left ventricular ejection fraction (EF), fractional shortenings (FS), left ventricular end diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD). (3) Ratio of left ventricular weight and body weight (LVW/BW) was calculated. (4) The expression levels of β₃-AR and SOCS3 mRNA in myocardium were detected by reverse transcription-polymerase chain reaction (RT-PCR). (5) The expression of SOCS3, Akt, pAkt and Caspase3 protein in myocardium were detected by western blot.

Results (1) Compared withIgroup, FS, LVEF was decreased and LVEDD, LVESD was increased inIIgroup; compared withIIgroup, FS, LVEF was increased and LVEDD, LVESD was decreased in IIIgroup. (2) Compared withIgroup, LVW/BW was increased inIIgroup, compared withIIgroup, LVW/BW was decreased in IIIgroup. (3) Compared withIgroup, β₃-AR and SOCS3 mRNA expression was increased in IIgroup; compared withIIgroup, β₃-AR and SOCS3 mRNA expression was decreased inIIIgroup. (4) Compared withIgroup, SOCS3, Caspase3 protein expression was increased and pAkt/Akt was decreased in IIgroup; compared withIII group, SOCS3, Caspase3 protein expression was decreased and pAkt/Akt was increased in III group.

Conclusions The expression of β₃-AR, SOCS3 and Caspase3 was increased, pAkt/Akt was decreased, cardiac performance was reduced and cell apoptosis was increased in heart failure rats; β₃-AR inhibitor may through SOCS3-pAkt/Akt-Caspase3 increase cardic function and decrease cell apoptosis, may provide a new signal path therapy for heart failure.