2006Chongqing yixueRequires access

Effects of captopril and valsartan on myocardial collagen remodeling in rats after myocardial infarction

MA Kang-hua

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Abstract

Objective To study the effects of captopril and valsartan on cardiac collagen net-work remodeling.Methods Twenty-nine SD rats were randomly divided into three groups:infracted group,captopril group and valsartan group.Except sham group,left anterior decending coronary artery was ligated.Hydroxyproline concerning collagen remodeling were observed and CT-1 mRNA and gp130 mRNA expression was tested by reverse transcription and polymerase chain reaction(RT-PCR).Results(1)HC was increased in infracted group,captopril and valsartan group compared with those in sham group.NIZ HC was decreased in captopril and valsartan group compared with infracted group(P0.05 or 0.01).(2)NIZ CT-1 mRNA and gp130 mRNA expression were increased in infracted group compared with those in sham group(P0.01).In valsartan group,expressions were remarkably decreased than in infracted group(P0.05).In captopril group CT-1 mRNA had no obvious chance(P0.05)and gp130 mRNA expression was decreased(P0.05).Conclusion Overexpression of CT-1 and gp130 may play an important role in CCN remodeling after MI,the mechanisms of valsartan preventing CCN remodeling may be partly through depressing CT-1 and gp130 overexpression,which is worth studying further.

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Objective To study the effects of captopril and valsartan on cardiac collagen net-work remodeling.Methods Twenty-nine SD rats were randomly divided into three groups:infracted group,captopril group and valsartan group.Except sham group,left anterior decending coronary artery was ligated.Hydroxyproline concerning collagen remodeling were observed and CT-1 mRNA and gp130 mRNA expression was tested by reverse transcription and polymerase chain reaction(RT-PCR).Results(1)HC was increased in infracted group,captopril and valsartan group compared with those in sham group.NIZ HC was decreased in captopril and valsartan group compared with infracted group(P0.05 or 0.01).(2)NIZ CT-1 mRNA and gp130 mRNA expression were increased in infracted group compared with those in sham group(P0.01).In valsartan group,expressions were remarkably decreased than in infracted group(P0.05).In captopril group CT-1 mRNA had no obvious chance(P0.05)and gp130 mRNA expression was decreased(P0.05).Conclusion Overexpression of CT-1 and gp130 may play an important role in CCN remodeling after MI,the mechanisms of valsartan preventing CCN remodeling may be partly through depressing CT-1 and gp130 overexpression,which is worth studying further.

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Available abstract

Objective To study the effects of captopril and valsartan on cardiac collagen net-work remodeling.Methods Twenty-nine SD rats were randomly divided into three groups:infracted group,captopril group and valsartan group.Except sham group,left anterior decending coronary artery was ligated.Hydroxyproline concerning collagen remodeling were observed and CT-1 mRNA and gp130 mRNA expression was tested by reverse transcription and polymerase chain reaction(RT-PCR).Results(1)HC was increased in infracted group,captopril and valsartan group compared with those in sham group.NIZ HC was decreased in captopril and valsartan group compared with infracted group(P0.05 or 0.01).(2)NIZ CT-1 mRNA and gp130 mRNA expression were increased in infracted group compared with those in sham group(P0.01).In valsartan group,expressions were remarkably decreased than in infracted group(P0.05).In captopril group CT-1 mRNA had no obvious chance(P0.05)and gp130 mRNA expression was decreased(P0.05).Conclusion Overexpression of CT-1 and gp130 may play an important role in CCN remodeling after MI,the mechanisms of valsartan preventing CCN remodeling may be partly through depressing CT-1 and gp130 overexpression,which is worth studying further.

Key concepts: Valsartan, Captopril, Messenger RNA, Internal medicine, Medicine, Ventricular remodeling, Endocrinology, Myocardial infarction

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Effects of captopril and valsartan on myocardial collagen remodeling in rats after myocardial infarction — Research Paper | ScholarLens