2011Medical Journal of West ChinaRequires access

Relationship between TGF-β_1/Smads signaling and ventricular remodeling after myocardial infarction in rats treated with simvastatin

Xuehua Wang

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Abstract

Objective To investigate the relationship between TGF-β1/Smads signaling and ventricular remodeling after myocardial infarction in rats treated with simvastatin.Methods 40 rats were randomly divided into four groups: Myocardial infarction group(MI,n=10) induced by left anterior descending coronary artery ligation in rats,sham-operated rats(Sham,n=10) used as control,simvastatin(Sim) treatment group(MI+Sim,n=10),Sim control group(Sim,n=10).The rats were sacrificed 8 weeks later.Heart weight/body weight(HW/BW),mean blood pres-sure,left ventricular end diastolic pressure(LVEDP),collagen content in un-infarcted area were examined.The mRNA levels of transforming growth factor(TGF)β1,Smad3 and Smad7 were determined by RT-PCR.Results The level of HW/BW,LVEDP and collagen content,the mRNA expression of TGF-β1 and Smad3 in areas of myocardial infarction and un-in-farction were significantly increased and the expression of Smad7 mRNA in these areas was decreased in MI group which compared with sham group and Sim group(P0.05).Conclusions These results indicates that TGFβ1-Smads signaling is correlated to the ventricular remodeling after myocardial infarction.Simvastatin may have a protective effect on ventricular remodeling after myocardial infarction.

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Objective To investigate the relationship between TGF-β1/Smads signaling and ventricular remodeling after myocardial infarction in rats treated with simvastatin.Methods 40 rats were randomly divided into four groups: Myocardial infarction group(MI,n=10) induced by left anterior descending coronary artery ligation in rats,sham-operated rats(Sham,n=10) used as control,simvastatin(Sim) treatment group(MI+Sim,n=10),Sim control group(Sim,n=10).The rats were sacrificed 8 weeks later.Heart weight/body weight(HW/BW),mean blood pres-sure,left ventricular end diastolic pressure(LVEDP),collagen content in un-infarcted area were examined.The mRNA levels of transforming growth factor(TGF)β1,Smad3 and Smad7 were determined by RT-PCR.Results The level of HW/BW,LVEDP and collagen content,the mRNA expression of TGF-β1 and Smad3 in areas of myocardial infarction and un-in-farction were significantly increased and the expression of Smad7 mRNA in these areas was decreased in MI group which compared with sham group and Sim group(P0.05).Conclusions These results indicates that TGFβ1-Smads signaling is correlated to the ventricular remodeling after myocardial infarction.Simvastatin may have a protective effect on ventricular remodeling after myocardial infarction.

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Available abstract

Objective To investigate the relationship between TGF-β1/Smads signaling and ventricular remodeling after myocardial infarction in rats treated with simvastatin.Methods 40 rats were randomly divided into four groups: Myocardial infarction group(MI,n=10) induced by left anterior descending coronary artery ligation in rats,sham-operated rats(Sham,n=10) used as control,simvastatin(Sim) treatment group(MI+Sim,n=10),Sim control group(Sim,n=10).The rats were sacrificed 8 weeks later.Heart weight/body weight(HW/BW),mean blood pres-sure,left ventricular end diastolic pressure(LVEDP),collagen content in un-infarcted area were examined.The mRNA levels of transforming growth factor(TGF)β1,Smad3 and Smad7 were determined by RT-PCR.Results The level of HW/BW,LVEDP and collagen content,the mRNA expression of TGF-β1 and Smad3 in areas of myocardial infarction and un-in-farction were significantly increased and the expression of Smad7 mRNA in these areas was decreased in MI group which compared with sham group and Sim group(P0.05).Conclusions These results indicates that TGFβ1-Smads signaling is correlated to the ventricular remodeling after myocardial infarction.Simvastatin may have a protective effect on ventricular remodeling after myocardial infarction.

Key concepts: Medicine, Simvastatin, Myocardial infarction, Ventricular remodeling, Internal medicine, Preload, Cardiology, Ligation

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