Effects Of Rosuvastatin On Expression Of PYARγ And NF-κB In Hypertrophic Myocardium Of Rat

ObjectiveTo investigate the effects of Rosuvastatin on peroxisome proliferator-activated receptor-γ(PPARγ) and p65subunit of nuclear factor-kappa B(NF-κB)in myocardial hypertrophy induced by isoproterenol(ISO) in rats and to investthe mechanism of rosuvastatin preventing hypertrophy and keeping cardiacfunction.Methods40healthy SD rats were randomly divided into control, model, rosuvastatinand captopril groups,10rats in each group. Myocardial hypertrophy modelswere induced by subcutaneous injection of ISO in which the dosage schedulewas set to20mg/kg in the1st day,10mg/kg in the2nd day,5mg/kg in the3rdday, and3mg/kg in the following consecutive seven days except for controlgroup. After the success of the model, rosuvastatin group were givenrosuvastatin4mg/(kg d), captopril group were given captopril50mg/(kg d), theother groups were given physiological saline. At the end of the experiment, thefollowing parameters were determined: left ventricular end-diastolic pressure(LVEDP), left ventricular systolic pressure (LVSP),±dp/dt max; body weight(BW), heart weight (HW), left ventricular wight(LVW), heart weight index(HWI),left ventricular wight index(LVWI); to observe the myocardial tissue morphologicchanges; PPARγand p65protein expression in cardiomyocyte nuclear wereanalyzed through immunohistochemical and Western blot. Results(1)Observation by light microscope, the normal control group,myocardialcells have normal form, the myocardial fibers in order, the myocardial tissuedoes not fibrosis;the model group compared with the normal control group,myocardial cells are arranged sparse, disorder, appear muscle bunch of fracture,fiber organizations of proliferation, interstitial obvious edema; rosuvastatin andcaptopril groups compared with model group, myocardial hypertrophy aresignificantly reduced, myocardial cells are arranged rules, fibre hyperplasiaextent lighter, interstitial mild edema.(2)LVEDP were significantly increased and LVSP、±dp/dt max weresignificantly decreased in model group than in control group(P＜0.01);rosuvastatin and captopril groups significantly decreased LVEDP(P＜0.05and P＜0.01)and increased LVSP、±dp/dt max than in model group(P＜0.05and P＜0.01).(3)HWI and LVWI were significantly increased in model group than incontrol group(P＜0.01); rosuvastatin and captopril groups significantlydecreased LVEDP than in model group(P＜0.01).(4)immunohistochemical: With the normal control group, the model groupincreased the protein of PPARγ and decreased the protein of p65(P＜0.01);rosuvastatin and captopril groups significantly decreased the protein ofPPARγ and increased the protein of p65(P＜0.01).(5)Western blot: With the normal control group, the model group decreasedthe protein of PPARγ and increased the protein of p65(P＜0.01);rosuvastatinand captopril groups significantly increased the protein of PPARγ anddecreased the protein of p65(P＜0.01).ConclusionsRosuvastatin inhibits the cardiac hypertrophy and improves cardiacfunction. The mechanism relates to the increase of PPARγ expression and decrease the p65expression.