Effects Of Valsartan On The Expression Of Caspase-3,8,9in Myocardial Tissue Of Spontaneously Hypertensive Rats And Study On Apoptosis

Background and aim of the study:With the development of hypertension, left ventricular hypertrophy is the foremost characteristic at the aspect of heart damage, which leads to heart failure ultimately. In numerous studies of mechanism which myocardial compensatory hypertrophy develops to heart failure, the phenomenon of apoptosis has been observed, which has been got more attention. Thus the present study aims to measure the activity of Caspase-3,8,9in the myocardial tissue of spontaneously hypertensive rat(SHR),to observer the effects of intervention of Valsartan, angiotensin Ⅱ type1receptor antagonist, and to investigate which way Valsartan influences activation of Caspase and cell apoptosis.Methods:(1)15SHRs were randomly grouped, and8of these rats were treated with Valsartan(30mg kg-1day-1) for8weeks. Therefore these15SHRs were divided into treatment group with Valsartan and non-treatment group, while we also set up normal control group (8WKY rats).After8weeks, the rats were killed, then we obtained left ventricular myocardial tissues. A portion of myocardial tissue were soaked in formaldehyde for6hours then embedded in paraffin, while other part of myocardial tissue stored in-80degrees of refrigerator after transferred to liquid nitrogen immediately.(2)We used the enzyme mark instrument for detecting the degree of activation of rats’myocardial Caspase-3,8,9respectively.(3) The paraffin sections were made for morphological study and TUNEL detection of apoptosis.Results:(1) The Caspase-3,8,9activity of the cardiac tissue decreased with the treatment of Valsartan, while Caspase-3,8,9activity of the non-treatment group was greater than that of the control group, the difference was significant (P<0.05).(2) The treatment of Valsartan mitigated damage in the myocardial tissue.(3) The treatment of Valsartan decreased the apoptosis index of myocardial tissue (P<0.05).Conclusions:Valsartan effectively decrease the activity of Caspase-3,8,9, and maybe inhibit myocardial apoptosis through death receptor-mediated extrinsic pathway and mitochondrial-mediated intrinsic pathway.