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Effect and Mechanism of Propranolol on the Myocardial Abnormal Electrophysiology Station in Diabetic Model Rats / 中国药房
China Pharmacy ; (12): 1357-1359, 2016.
Article in Chinese | WPRIM | ID: wpr-504427
ABSTRACT

OBJECTIVE:

To study the effects and mechanism of propranolol on the myocardial abnormal electrophysiology sta-tion in diabetic model rats.

METHODS:

SD rats were randomly divided into normal control(normal saline)group,diabetic(nor-mal 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 car-diac 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 myocar-dial abnormal electrophysiology station of diabetic model rats by down-regulating inflammatory reactions in serum and inhibiting the activation of MEK/ERK signaling pathway.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: China Pharmacy Year: 2016 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: China Pharmacy Year: 2016 Type: Article