The Role Of CaMKⅡ δ And The Gene Apoptosis With Bcl-2and Bax In Myocardial Hypertrophy

ObjectiveThis paper aims to explore the expressing rules and mutual relationship between CaMKⅡδand apoptosis gene bcl-2bax in the issue of myocardial hypertrophy, and to make clear the regulation mechanism of CaMK Ⅱδ in cell apoptosis, which works for providing a new approach to develop new drugs in clinical research and development to prevent myocardial hypertrophy and reduce myocardial cell apoptosis.Methods1.40New Zealand rabbits were divided into the groups of treatment and control randomly, each group has20rabbits. The group of treatment had surgery by narrowing the abdominal aorta to set up the module of myocardial hypertrophy, and the control group was operated just by opening, instead of teroding the abdominal aorta. Put the rabbits to death and enrolled the biometrics heart specimens after ensure the success of the models by heart ultrasound after8weeks.2. Detected the CaMKⅡδ、 bcl-2and bax in the hearts tissue of the groups of treatment and control by fluorescent quantitative PCR test.3. Contrasted the change and the correlation of CaMKⅡδ、 bcl-2and bax in the hearts tissue of the groups of treatment and control by statistical analysis.Results1. The treatment group rabbits all appeared myocardial hypertrophy obviously after8weeks of surgery, of which the IVS and LVPW thickened obviously (P＜0.05), and the EF、 LVDd、 LVDs had no changing signifieantly (P＞0.05), but the control group did not change. 2. Compared with the control group, the expression of CaMK Ⅱδ in myocardial tissue of the treatment group increased significantly (P＜0.01).3. Compared with the control group, the expression of bcl-2in myocardial tissue of the treatment group decreased but the expression of bax increased (P＜0.05), and the ratio of bcl-2/bax decreased evidently (P＜0.05).4. As far as the treatment group was concerned, the increasing of CaMK Ⅱδ was significantly associated with the decreasing of the ratio of bcl-2/bax. However, the control group did not have obvious correlation.Conclusion1. The way of establishing the model of myocardial hypertrophy by narrowing the abdominal aorta is effective, echocardiography can reflect the extent of the myocardial hypertrophy relatively well, which perform in thickening of LVPW and IVS.The model also shows the rabbits all appeared left ventricular hypertrophy, and8weeks was enough for the models, while needs more time to develop to heart failure.2. Signal transduction pathway of CaMK Ⅱδ is an important part of myocardial hypertrophy, and the increasing expression of CaMK Ⅱδ may induce cell apoptosis more by lowering bcl-2/bax, which cause myocardial hypertrophy together.