Effect and Mechanism of Propranolol on the Myocardial Abnormal Electrophysiology Station in Diabetic Model Rats
10.6039/j.issn.1001-0408.2016.10.18
- VernacularTitle:普萘洛尔对糖尿病模型大鼠心肌异常电生理效果的影响及机制
- Author:
Jun LIU
;
Xin WANG
;
Ji DENG
;
Jing JIA
;
Jing XIAO
- Publication Type:Journal Article
- Keywords:
Diabetes;
Propranolol;
Myocardial abnormality;
Electrophysiology station;
MEK/ERK signaling pathway;
Inflam-matory reaction;
Rats
- From:
China Pharmacy
2016;27(10):1357-1359
- CountryChina
- Language:Chinese
-
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.
