Effect Of Atorvastatin On Expression Of CTGF、NF-κB In Hypertrophic Myocardium Of Rats By Pressure Overland-induced

ObjectiveTo investigate the differential dxpression of connective tissue growthfactor(CTGF) and nuclear factorκB(NF-κB) between normal rats and rats ofcardiac hypertrophy model produced by abdominal aortic banding,and effects ofAtorvastatin on the expression of CTGF and NF-κB to explore the mechanism.Methods40male SD rats were randomly divided into4groups,sham-operatedgroup (n=10),model group (n=10),Atorvastatin group [5mg/(kg·d),(n=10)] andCaptopril group[50mg/(kg·d),(n=10)].all the rats except of sham-operated groupwere made to be myocardial hypertrophy model produced by abdominal aorticbanding,sham-operated group ones were given a suture line under the arterywithout banding.24h after operation，the rats of Atorvastatin group were given adaily dose of5mg/kg of Atorvastatin which was dissolved in1ml normal salineby gastric gavage, the rats of Captopril group were given a daily dose of50mg/kg of Captopril, and same volume normal saline given to the other twogroups respectively,After6weeds,record the extent and hemodynamicperformance of hypertrophic myocardium by the interventricular septalthickness(IVST)、left ventricular posterior wall thickness(LVPWT);systolic bloodpressure(SBP)、diastolic blood pressure(DBP)、left ventricular end-diastolic pressure(LVEDP)、The maximum rising and falling velocity of left ventricularpressure (±dp/dtmax);body weight(BW), than the animals were killed to take leftventricular weight (HW)、left ventricular weight(LVW)、left ventricular weightindex(LVWI)； Myocardial tissue on the linght microscope morphological、immunohistochemical detection and Western blot detection for CTGF andNF-κB in qualitative and quantitative expression.Results1.Compared with the sham-operated group, the rest three groups’ IVST、LVPWT、SBP、DBP、LVEDP and LVWI levels were significantly higher(P﹤0.05),±dp/dtmaxlevel decreased significantly(P﹤0.05)； with the model group，Atorvastatin group’ s IVST、LVPWT、LVWI levels were significantly lower(P﹤0.05), SBP、 DBP、 LVEDP were a little lower(P﹥0.05),±dp/dtmaxlevelsignificantly higher (P﹤0.05); with the model group,Captopril group’ s IVST、LVPWT、SBP、DBP、LVEDP、LVWI levels were significantly lower(P﹤0.05)，±dp/dtmaxa little higher(P﹥0.05)；2.HE-stained：through the high-intensity illumination optical microscope，thesham-operated group，myocardial cells detected a normal morphology, cardiacfibers layered clear,without myocardium fibrosis; Compared with thesham-operated group, model group’ s myocardial cells layered disordered andscattered, fractured muscle, plentiful of fibrous tissue, Interstitial cells edemacould be seen; Compared with the sham-operated group, Atorvastatin groupand Captopril group’ s myocardial cells layered clear, Interstitial cells were mildedema.3.Immunohistochemistry showed that: compared with the sham-operatedgroup，model group’ s gray value of CTGF and NF-κB were significantly lower(P﹤0.05); with the model group, Atorvastatin group and Captopril group’ s grayvalue were significantly higher(P﹤0.05);Differences between Atorvastatingroup and Captopril group where was no statistical significance(P﹥0.05). 4.Western blot showed that: compared with the sham-operated group，model group’ s CTGF and NF-κB level were significantly higher(P﹤0.05); withthe model group, Atorvastatin group and Captopril group’ s level weresignificantly lower (P﹤0.05);With the Captopril group, Atorvastatin group’ sCTGF was significantly higher (P﹤0.05),but for NF-κB where was no statisticalsignificance(P﹥0.05).ConclusionsAtorvastatin obviously inhibits the rats’ cardiac hypertrophy, Themechanism relates may depend on restraining the expression of CTGF andNF-κB.