Effect Of L-canitine On TGF-β1/Smad3 Signal Pathway And Myocardial Energy Metabolism On Myocardial Hypertrophy In Rats

PurposeTo research the effect of L-canitine on TGF-β1/Smad3 signal pathway and myocardial energy metabolism on isoprenaline-induced myocardial hypertrophy in rats and discuss its related mechanism.MethodsForty healthy SD rats were randomly divided into four group:blank control group(group A),model group(group B),L-carnitine 50 mg/kg group(group C1)and L-carnitine 100 mg/kg group(group C2).The rats of B,C1 and C2 groups were established mycatdial hypertrophy mode by subcutaneous injection of5mg/(kg?d)isoproretnol(Iso)for 10 days.The rats of C1 group and C2 group were respectively given 50 mg/(kg?d)and 100 mg/(kg?d)L-carnitine by intraperitoneal injection for eight weeks from the second day of subcutaneous injection of Iso.Then the left ventricular ejection fractions(LVEF),heart mass index(HMI)and left ventricular mass index(LVMI)were measured.Myocardial cells were observed under light microscope by HE staining.The free fatty acids(FFA),lactate acids(LAC)and adenosine triphosphate(ATP)contents in myocardial tissue of rats were detected,and the expression of TGF-β1 and Smad3 protein were detected by Western Blot.ResultsThe LVEF of model group,L-carnitine 50 mg/kg and 100 mg/kg groups both diminished signi?cantly and the HMI and LVMI increased obviously when compared to blank control group(P<0.05),myocardial cells were more hypertrophied and its structure became more disorder compared to blank control group,the content of FFA and LAC were higher than blank control group while ATP decreased(P<0.05),and the expression of TGF-β1 and Smad3 protein increased signi?cantly(P<0.05).The LVEF and content of ATP rised signi?cantly while all other indexes decreased cleartly in L-carnitine 50 mg/kg and 100 mg/kg groups when compared with model group(P<0.05),The result of100 mg/kg groups vary markedly(P<0.05).ConclusionL-carnitine can improve the energy metabolism of myocardial hypertrophy and reduce the expression of TGF-β1 and Smad3 protein,prompting it inhibited myocardial hypertrophy by improving myocardial energy metabolism and restraining TGF-β1/Smad3 signal pathway.