2011China Medical HeraldRequires access

The effection of Tanshinone on calcineurin expression in myocardial hypertrophy organization

Le Yang

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Abstract

Objective: To explore the relationship between Tanshinone resistance left ventricular remodeling and calcineurin signal pathway by the rat models of myocardial hypertrophy which were caused by abdominal aortic coarctation.Methods: SD rats were operated with abdominal aorta constriction to construct the model of myocardial hypertrophy.After 4 weeks,model rats were divided into four groups: artificial operation group(group B),low dose Tanshinone group [group C,10 mg/(kg·d)],high dose Tanshinone group [group D,20mg/(kg·d)] and Valsartan group [group E,10mg/(kg·d)],each of 8 cases and 8 rats were divided into sham operation group(group A).8 weeks later,tail arterial pressure and the left ventricular mass index(LVMI) were measured,and myocardial fiber dimension(MFD) which were stained with HE reagent also was measured.AT1 receptor mRNA expression was detected by RT-PCR.AT1 receptor and CaN protein expression were detected by western blotting in left ventricular tissues of all groups.i was observed by Fura-2 double wavelengths fluorescence method.Results: The blood pressure in group B,C,D were obviously higher than that in group A and group E,the difference was statistically significant(P0.01),But there was no statistical difference between group B,C and D(P0.05).The LVMI and MFD vaule were obviously higher in group C,D,E than that of group A,and lower than that of group B,the differences were statistically significant(P0.05).The protein and mRNA expression of AT1 receptor in group B were the highest in all groups,the differences were statistically significant(P0.01),and there was no statistical different between group C and D(P0.05),which was higher than group E,the difference was statistically significant(P0.05).But the mRNA expression in group C,D and E were not recovered to the normal level(group A),the differences were statistically significant(P0.05).The protein expression of CaN in group B was obviously higher than that of other groups,the differences were statistically significant(P0.05),and the interventions of Tanshinone were dose-dependent.There was no statistical difference between group D and group E(P0.05).The concentration of i in group B was higher than other groups,the differences were statistically significant(P0.01),and there was no statistical difference between group D and group A(P0.05),but the concentration of i in group E and group C were higher than that of group A and D,the differences were statistically significant(P0.05).Conclusion: Tanshinone can resist the myocardial hypertrophy by blocking the inflow of calciumion and downregulating the protein expression of CaN in cadiocyte.

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Objective: To explore the relationship between Tanshinone resistance left ventricular remodeling and calcineurin signal pathway by the rat models of myocardial hypertrophy which were caused by abdominal aortic coarctation.Methods: SD rats were operated with abdominal aorta constriction to construct the model of myocardial hypertrophy.After 4 weeks,model rats were divided into four groups: artificial operation group(group B),low dose Tanshinone group [group C,10 mg/(kg·d)],high dose Tanshinone group [group D,20mg/(kg·d)] and Valsartan group [group E,10mg/(kg·d)],each of 8 cases and 8 rats were divided into sham operation group(group A).8 weeks later,tail arterial pressure and the left ventricular mass index(LVMI) were measured,and myocardial fiber dimension(MFD) which were stained with HE reagent also was measured.AT1 receptor mRNA expression was detected by RT-PCR.AT1 receptor and CaN protein expression were detected by western blotting in left ventricular tissues of all groups.i was observed by Fura-2 double wavelengths fluorescence method.Results: The blood pressure in group B,C,D were obviously higher than that in group A and group E,the difference was statistically significant(P0.01),But there was no statistical difference between group B,C and D(P0.05).The LVMI and MFD vaule were obviously higher in group C,D,E than that of group A,and lower than that of group B,the differences were statistically significant(P0.05).The protein and mRNA expression of AT1 receptor in group B were the highest in all groups,the differences were statistically significant(P0.01),and there was no statistical different between group C and D(P0.05),which was higher than group E,the difference was statistically significant(P0.05).But the mRNA expression in group C,D and E were not recovered to the normal level(group A),the differences were statistically significant(P0.05).The protein expression of CaN in group B was obviously higher than that of other groups,the differences were statistically significant(P0.05),and the interventions of Tanshinone were dose-dependent.There was no statistical difference between group D and group E(P0.05).The concentration of i in group B was higher than other groups,the differences were statistically significant(P0.01),and there was no statistical difference between group D and group A(P0.05),but the concentration of i in group E and group C were higher than that of group A and D,the differences were statistically significant(P0.05).Conclusion: Tanshinone can resist the myocardial hypertrophy by blocking the inflow of calciumion and downregulating the protein expression of CaN in cadiocyte.

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Available abstract

Objective: To explore the relationship between Tanshinone resistance left ventricular remodeling and calcineurin signal pathway by the rat models of myocardial hypertrophy which were caused by abdominal aortic coarctation.Methods: SD rats were operated with abdominal aorta constriction to construct the model of myocardial hypertrophy.After 4 weeks,model rats were divided into four groups: artificial operation group(group B),low dose Tanshinone group [group C,10 mg/(kg·d)],high dose Tanshinone group [group D,20mg/(kg·d)] and Valsartan group [group E,10mg/(kg·d)],each of 8 cases and 8 rats were divided into sham operation group(group A).8 weeks later,tail arterial pressure and the left ventricular mass index(LVMI) were measured,and myocardial fiber dimension(MFD) which were stained with HE reagent also was measured.AT1 receptor mRNA expression was detected by RT-PCR.AT1 receptor and CaN protein expression were detected by western blotting in left ventricular tissues of all groups.i was observed by Fura-2 double wavelengths fluorescence method.Results: The blood pressure in group B,C,D were obviously higher than that in group A and group E,the difference was statistically significant(P0.01),But there was no statistical difference between group B,C and D(P0.05).The LVMI and MFD vaule were obviously higher in group C,D,E than that of group A,and lower than that of group B,the differences were statistically significant(P0.05).The protein and mRNA expression of AT1 receptor in group B were the highest in all groups,the differences were statistically significant(P0.01),and there was no statistical different between group C and D(P0.05),which was higher than group E,the difference was statistically significant(P0.05).But the mRNA expression in group C,D and E were not recovered to the normal level(group A),the differences were statistically significant(P0.05).The protein expression of CaN in group B was obviously higher than that of other groups,the differences were statistically significant(P0.05),and the interventions of Tanshinone were dose-dependent.There was no statistical difference between group D and group E(P0.05).The concentration of i in group B was higher than other groups,the differences were statistically significant(P0.01),and there was no statistical difference between group D and group A(P0.05),but the concentration of i in group E and group C were higher than that of group A and D,the differences were statistically significant(P0.05).Conclusion: Tanshinone can resist the myocardial hypertrophy by blocking the inflow of calciumion and downregulating the protein expression of CaN in cadiocyte.

Key concepts: Medicine, Valsartan, Internal medicine, Irbesartan, Muscle hypertrophy, Angiotensin II receptor type 1, Group A, Receptor

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