Zhonghua xin xue guan bing za zhi · 2009
[The effects of simvastatin on cardiac hypertrophy and association on calcium channel modulation in rats with myocardial hypertrophy induced by abdominal aortic constriction].
Аннотация на английскомСтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wu Yang, Yang Hui-chao, Chen Xiang
Аннотация
OBJECTIVE: To investigate the effects of simvastatin (SIM)on cardiac hypertrophy and association with calcium channel modulation in rats with myocardial hypertrophy.
METHODS: Myocardial hypertrophy was induced by abdominal aortic constriction (AAC) in adult SD rats. Following groups were studied (n=8 each): sham group, AAC group, AAC+ verapamil group (10 mg x kg(-1) x d(-1) per gavage for 4 weeks), AAC +SIM group (10 mg x kg(-1) x d(-1) per gavage for 4 weeks) AAC + SIM + mevalonic acid (50 mg x kg(-1) x d(-1) per gavage for 4 weeks) group. Systolic blood pressure (SBP), echocardiography, heart weight/body weight (HW/BW) and left ventricle weight/body weight (LVW/BW) ratios were measured. The protein and mRNA expressions of L-type calcium channel subunit alpha1 C and T-type calcium channel subunit alpha1 G and alpha1 H were detected by Western blot and RT-PCR respectively.
RESULTS: SBP, HW/BW, LVW/BW, IVS and LVPW thickness, left ventricular weights were significantly increased in AAC rats and these effects could be significantly reduced by verapamil and SIM. The protein and mRNA expressions of alpha1 G and alpha1 H were significantly increased in AAC rats which could also be significantly inhibited by SIM or verapamil. The effects of SIM could be blocked by cotreatment with mevalonic acid. Protein and mRNA expressions of L-type calcium channel alpha1 C were similar among groups.
CONCLUSION: Similar as verapamil, SIM could prevent AAC induced cardiac hypertrophy, possibly via inhibiting T-type calcium channel subunit alpha1 G and alpha1 H re-expression.
METHODS: Myocardial hypertrophy was induced by abdominal aortic constriction (AAC) in adult SD rats. Following groups were studied (n=8 each): sham group, AAC group, AAC+ verapamil group (10 mg x kg(-1) x d(-1) per gavage for 4 weeks), AAC +SIM group (10 mg x kg(-1) x d(-1) per gavage for 4 weeks) AAC + SIM + mevalonic acid (50 mg x kg(-1) x d(-1) per gavage for 4 weeks) group. Systolic blood pressure (SBP), echocardiography, heart weight/body weight (HW/BW) and left ventricle weight/body weight (LVW/BW) ratios were measured. The protein and mRNA expressions of L-type calcium channel subunit alpha1 C and T-type calcium channel subunit alpha1 G and alpha1 H were detected by Western blot and RT-PCR respectively.
RESULTS: SBP, HW/BW, LVW/BW, IVS and LVPW thickness, left ventricular weights were significantly increased in AAC rats and these effects could be significantly reduced by verapamil and SIM. The protein and mRNA expressions of alpha1 G and alpha1 H were significantly increased in AAC rats which could also be significantly inhibited by SIM or verapamil. The effects of SIM could be blocked by cotreatment with mevalonic acid. Protein and mRNA expressions of L-type calcium channel alpha1 C were similar among groups.
CONCLUSION: Similar as verapamil, SIM could prevent AAC induced cardiac hypertrophy, possibly via inhibiting T-type calcium channel subunit alpha1 G and alpha1 H re-expression.