ABSTRACT
OBJECTIVE: To observe the inhibitiory effect of adenosine A1 receptor stimulation on myocardial hypertrophy by TGF-β1/Smad3 signal pathways and myocardial energy metabolism in rats and discuss its related mechanism. METHODS: High dose isoproterrnol was subcutaneously injected into rats to establish myocardial hypertrophy model. Forty Sprague-Dawley rats were randomly divided into four groups with ten rats for each group:blank control group,isoproterenol model group, CCPA(150 μg·kg-1·min-1) treatment group.From second day after modeling,rats in CCPA group and in propranolol group were injected continuosly for eight weeks. Then the heart mass index (HMI)and left ventricular mass index (LVMI) were measured, the myocardial cells were observed under the light microscope by HE staining. The free fatty acids (FFA), lactic acids (LAC) and adenosine triphosphate (ATP) contents in myocardial tissue of rats were detected. The relative expression of TGE-β1 and Smad3 protein were determined by Western blotting. RESULTS: Compared with model group, in CCPA group, the HMI and LVMI were reduced, the conetent of FFA and LAC were decreased, the content of ATP was increased,and the relative expression of TGF-β1/Smad3 of CCPA group was decreased. CONCLUSION: When the adenosine A1 receptor was stimulated, it can improve the energy metabolism of myocardial hypertrophy, and restrain TGF-β1/Smad3 signal pathway, thus it play a protective role in the myocardial cells by reducing the expression of TGF-β1 and Smad3 protein.