Effects Of Tanshinone ⅡA On Myocardial Hypertrophy Signal Transduction System Protein Kinase B

PartⅠThe establishment and evaluation of rat model of myocardial hypertrophythrough adopting partial coarctation in the thoracic aortaObjective:To explore the validity and reliability of experimental ratmodel of myocardial hypertrophy through adopting partial coarctation in the thoracicaorta.Methods:The rat model of myocardial hypertrophy was established by adoptingpartial coarctation in the thoracic aorta,and detected respectively heart mass index(HMI),left ventricular mass index(LVMI),left ventricular posterior wall and septumthickness(LVPW,IVS) by highfrequenty ultrasonography,myocardial fiberdiameter(MFD) by HE staining.Results:The rat model of myocardial hypertrophy hasbeen established successfully for 10 weeks.Compared with the sham group,heart massindex,left ventricular mass index,left ventricular posterior wall and septumthickness were increased,and myocardial fiber diameter were higher in model group.Conclusions:The rat model of pressure overload myocardial hypertrophy can beestablished successfully by adopting partial coarctation in the thoracic aorta.PartⅡEffects of TanshinoneⅡA on myocardial signal transduction systemprotein kinase B in rat model of myocardial hypertrophy throughadopting partial coarctation in the thoracic aortaObjective:To explore the effects of tanshinoneⅡA on cell signaltransduction system protein kinase B in rats with pressure overload myocardialhypertrophy through adopting partial coarctation in the thoracic aorta.Methods:The ratmodel of myocardial hypertrophy was established by adopting partial coarctation in thethoracic aorta,and detected respectively the content of p-Akt,p-Gsk3βin myocardiumby western blot in sham group(group S),model group(group M),valsartan treatmentgroup(group X),low-dose tanshinone treatment group(group LD),medium-dosetanshinone treatment group(group MD),high-dose tanshinone treatment group (groupHD).Results:Compared with the sham group,the contents of p-Akt and p-Gsk3βwere increased in model group and all treatment groups.Compared with modelgroup,the contents of p-Akt and p-Gsk3βwere decreased in the valsartan treatmentgroup and all dose tanshinone treatment groups.But there were no significant differenceamong the low,medium,high-dose tanshinone treatment group,and there were nosignificant difference among the valsartan treatment group and all dose tanshinonetreatment group.Conclusions:When the myocardium cell signal transduction systemprotein kinase B in the rat is inactivated,it can induce to the myocardial hypertrophy.And TanshinoneⅡA can act on the protein kinase B(Akt) signaling pathway,toprevent myocardial hypertrophy.PartⅢThe establishment and evaluation of rat model of myocardial hypertrophythrough adopting partial coarctation in the abdominal aortaObjective:To explore the validity and reliability of experimental ratmodel of myocardial hypertrophy through adopting partial coarctation in the abdominalaorta.Methods:The rat model of myocardial hypertrophy was established by adoptingpartial coarctation in the abdominal aorta,and detected respectively tail artery systolicblood pressure(SBP) and heart mass index(HMI),left ventricular massindex(LVMI),left ventricular posterior wall and septum thickness(LVPW,IVS) byhighfrequenty ultrasonography,myocardial fiber diameter(MFD) by HE staining.Results:The rat model of myocardial hypertrophy has been established successfully for10 weeks.Compared with the sham group,tail artery systolic blood pressure,heartmass index,left ventricular mass index,left ventricular posterior wall and septumthickness were increased,and myocardial fiber diameter were higher in model group.Conclusions:The rat model of pressure overload myocardial hypertrophy can beestablished successfully by adopting partial coarctation in the abdominal aorta. PartⅣEffects of TanshinoneⅡA on myocardial signal transduction systemprotein kinase B in rat model of myocardial hypertrophy throughadopting partial coarctation in the abdominal aortaObjective:To explore the effects of tanshinoneⅡA on cell signaltransduction system protein kinase B in rats with pressure overload myocardialhypertrophy through adopting partial coarctation in the abdominal aorta.Methods:Therat model of myocardial hypertrophy was established by adopting partial coarctation inthe abdominal aorta,and detected respectively the content of p-Akt,p-Gsk3βinmyocardium by western blot in sham group(group S),model group(group M),valsartan treatment group(group X),low-dose tanshinone treatment group(groupLD),medium-dose tanshinone treatment group(group MD),high-dose tanshinonetreatment group(groupHD).Results:Compared with the sham group,the contents of p-Akt and p-Gsk3βwere increased in model group and all treatment groups.Comparedwith model group,the contents of p-Akt and p-Gsk3βwere decreased in the valsartantreatment group and all dose tanshinone treatment groups.But there were no significantdifference among the low,medium,high-dose tanshinone treatment group,and therewere no significant difference among the valsartan treatment group and all dosetanshinone treatment group.Conclusions:When the myocardium cell signaltransduction system protein kinase B in the rat is inactivated,it can induce to themyocardial hypertrophy.And TanshinoneⅡA can act on the protein kinase B(Akt)signaling pathway,to prevent myocardial hypertrophy.