OBJECTIVE： To study the effects and mechanism of propranolol on the myocardial abnormal electrophysiology station in diabetic model rats. METHODS： SD rats were randomly divided into normal control （normal saline） group， diabetic （normal saline） group， PD98059 （ERK inhibitor， 10 mg/kg） group and propranolol low-dose， medium-dose and high-dose （1， 20， 50 mg/kg） groups， with 8 rats in each group. Except for normal control group， rats were given alloxan （20 mg/kg） intravenously via tail vein to induce diabetic model. They were given relevant medicine intragastrically， once a day， for consecutive 42 days. The cardiac index， electrocardiogram and action potential durations （APD） of rats were analyzed； the expression of TNF-α， IL-2， IL-6 and IL-10 protein in serum were detected， and the expression of Ras， Raf， ERK kinase （MEK） and ERK1/2 in myocardial tissue were detected. RESULTS： Compared with normal control group， cardiac index increased in diabetes group； heart rate decreased； QT interval and APD were prolonged； the relative expression of TNF-α， IL-2， IL-6， IL-10， Ras， Raf， MEK and ERK1/2 protein increased （P＜0.01）. Compared with diabetes group， cardiac index decreased in propranolol medium-dose and high-dose groups and PD98059 group， heart rate increased， QT interval and APD were shortened； the relative expression of TNF-α， IL-2， IL-6， IL-10， Ras， Raf， MEK and ERK1/2 protein decreased （P＜0.05 or P＜0.01）. CONCLUSIONS： Propranolol can improve myocardial abnormal electrophysiology station of diabetic model rats by down-regulating inflammatory reactions in serum and inhibiting the activation of MEK/ERK signaling pathway.