2012Zhonghua linchuang yishi zazhiRequires access

Effects of osthole postconditioning on cardiomyocyte apoptosis induced by acute ischemia/reperfusion in rats and the possible mechanism

Liang Fen

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Abstract

Objective To investigate the effects of Osthole postconditioning on cardiomyocyte apoptosis induced by ischemia/reperfusion in rats,and to study the possible mechanism.Methods The acute myocardial ischemia/reperfusion rat models were established by ligating anterior decending branch of left coronary artery for 30 min and then reperfused 120 min.30 Wistar rats were randomly divided into Control(Sham)group,Ischemia/reperfusion(I/R)group and I/R+Osthole postconditioning(Ost)group.Cardiomyocyte apoptosis was determined by TUNEL staining and Caspase-3 expression.The expressions of Caspase-3,Bcl-2 and Bax protein in the myocardium were detected by Western blot technique.Results Compared with the Sham group,the apoptotic index(AI),the expression of Caspase-3,Bcl-2 and Bax protein in myocardial tissues were significantly increased in I/R group(P0.05).Compared with I/R group,the apoptotic index(AI)(P0.05),the expression of Caspase-3(P0.01)and Bax protein in myocardial tissues(P0.05)was decreased significantly,while Bcl-2 protein(P0.05)was increased significantly in Ost group.Conclusions The present study find that Osthole postconditioning decrease cardiomyocyte apoptosis induced by acute ischemia/reperfusion injury in rats,up-regulate the expression of Bcl-2 protein and down-regulate the expression of Bax protein,which suggest the cardioprotection effects of osthole postconditioning might be associated with up-regulating the expression of Bcl-2 protein,down-regulating the expression of Bax protein,and then raising the ratio of Bcl-2/Bax.

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Objective To investigate the effects of Osthole postconditioning on cardiomyocyte apoptosis induced by ischemia/reperfusion in rats,and to study the possible mechanism.Methods The acute myocardial ischemia/reperfusion rat models were established by ligating anterior decending branch of left coronary artery for 30 min and then reperfused 120 min.30 Wistar rats were randomly divided into Control(Sham)group,Ischemia/reperfusion(I/R)group and I/R+Osthole postconditioning(Ost)group.Cardiomyocyte apoptosis was determined by TUNEL staining and Caspase-3 expression.The expressions of Caspase-3,Bcl-2 and Bax protein in the myocardium were detected by Western blot technique.Results Compared with the Sham group,the apoptotic index(AI),the expression of Caspase-3,Bcl-2 and Bax protein in myocardial tissues were significantly increased in I/R group(P0.05).Compared with I/R group,the apoptotic index(AI)(P0.05),the expression of Caspase-3(P0.01)and Bax protein in myocardial tissues(P0.05)was decreased significantly,while Bcl-2 protein(P0.05)was increased significantly in Ost group.Conclusions The present study find that Osthole postconditioning decrease cardiomyocyte apoptosis induced by acute ischemia/reperfusion injury in rats,up-regulate the expression of Bcl-2 protein and down-regulate the expression of Bax protein,which suggest the cardioprotection effects of osthole postconditioning might be associated with up-regulating the expression of Bcl-2 protein,down-regulating the expression of Bax protein,and then raising the ratio of Bcl-2/Bax.

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Available abstract

Objective To investigate the effects of Osthole postconditioning on cardiomyocyte apoptosis induced by ischemia/reperfusion in rats,and to study the possible mechanism.Methods The acute myocardial ischemia/reperfusion rat models were established by ligating anterior decending branch of left coronary artery for 30 min and then reperfused 120 min.30 Wistar rats were randomly divided into Control(Sham)group,Ischemia/reperfusion(I/R)group and I/R+Osthole postconditioning(Ost)group.Cardiomyocyte apoptosis was determined by TUNEL staining and Caspase-3 expression.The expressions of Caspase-3,Bcl-2 and Bax protein in the myocardium were detected by Western blot technique.Results Compared with the Sham group,the apoptotic index(AI),the expression of Caspase-3,Bcl-2 and Bax protein in myocardial tissues were significantly increased in I/R group(P0.05).Compared with I/R group,the apoptotic index(AI)(P0.05),the expression of Caspase-3(P0.01)and Bax protein in myocardial tissues(P0.05)was decreased significantly,while Bcl-2 protein(P0.05)was increased significantly in Ost group.Conclusions The present study find that Osthole postconditioning decrease cardiomyocyte apoptosis induced by acute ischemia/reperfusion injury in rats,up-regulate the expression of Bcl-2 protein and down-regulate the expression of Bax protein,which suggest the cardioprotection effects of osthole postconditioning might be associated with up-regulating the expression of Bcl-2 protein,down-regulating the expression of Bax protein,and then raising the ratio of Bcl-2/Bax.

Key concepts: Apoptosis, Cardioprotection, TUNEL assay, Ischemia, Western blot, BAX Protein, Medicine, Reperfusion injury

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