Effects of carvedilol at different doses on cardiac myocyte apoptosis and apoptosis-associated gene in rats with pressure overload
Da Ye
Abstract
Da Ye
Abstract
AIM: To study the effects and mechanism of carvedilol (CAR) at different doses on cardiac myocyte apoptosis in rats with myocardial hypertrophy of CHF. METHODS: Using the animal model of CHF, induced by abdominal aortic constriction in male Wistar rats, hemodyanmics parameters, cardiac myocyte apoptosis, and the expression of Bcl-2 and P53 were investigated in the untreated experimental group (CHF group) at 1 week after operation and treated experimental groups in which rats were treated with CAR at a lower dose (LCAR group, 0.1 mg·kg -1·d -1) and at a higher dose (HCAR group, 10 mg·kg -1·d -1) for 7 weeks since 1 week after operation. The sham-operated rats were as controls (SH group, n=8). RESULTS: Either doses improved heart function and decreased apoptosis index in rats with CHF. The number of myocytes apoptosis and the level of Bcl-2 were significantly higher and P53 was markedly lower in HCAR group than those in LCAR and MCAR groups. CONCLUSION: CAR can effectively decrease myocardiocyte apoptosis, prevent and cure CHF. The effects are dose-dependent, associated with changes of the expression of apoptosis-associated gene.
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AIM: To study the effects and mechanism of carvedilol (CAR) at different doses on cardiac myocyte apoptosis in rats with myocardial hypertrophy of CHF. METHODS: Using the animal model of CHF, induced by abdominal aortic constriction in male Wistar rats, hemodyanmics parameters, cardiac myocyte apoptosis, and the expression of Bcl-2 and P53 were investigated in the untreated experimental group (CHF group) at 1 week after operation and treated experimental groups in which rats were treated with CAR at a lower dose (LCAR group, 0.1 mg·kg -1·d -1) and at a higher dose (HCAR group, 10 mg·kg -1·d -1) for 7 weeks since 1 week after operation. The sham-operated rats were as controls (SH group, n=8). RESULTS: Either doses improved heart function and decreased apoptosis index in rats with CHF. The number of myocytes apoptosis and the level of Bcl-2 were significantly higher and P53 was markedly lower in HCAR group than those in LCAR and MCAR groups. CONCLUSION: CAR can effectively decrease myocardiocyte apoptosis, prevent and cure CHF. The effects are dose-dependent, associated with changes of the expression of apoptosis-associated gene.
Key concepts: Apoptosis, Carvedilol, Myocyte, Medicine, Cardiac myocyte, Cardiac function curve, Pressure overload, Endocrinology