Effect of Cyclosporine A on the Right Ventricle Remodeling in Monocrotaline-Treated Rats
Su Min
Abstract
Su Min
Abstract
OBJECTIVE To explore the effect and the preliminary mechanism of cyclosporine A (CsA) on the right ventricle remodeling caused by monocrotaline (MCT). METHODS Thirty-six Sprague-Dawley male rats were randomly divided into normal control group,MCT group,low and high dose of CsA treatment group. Rats were given a single dose of MCT (50 mg·kg-1, sc) for inducing the right ventricle remodeling. CsA (0.33 and 1 mg·kg-1,bid,ig) was administered from day 14 to day 21 respectively. The right ventricle (RV) and the left ventricle with septum (LV+SEP) were weighed separately. RVHI was measured as RV/(LV+SEP). The histological examination of RV were executed by light microscope. The ultramicrostructure of the RV tissues was observed under the transmission electron microscope. Immunohistochemical analysis was performed on paraffin-embedded RV tissue using the anti-proliferating cell nuclear antigen (PCNA) primary antibodies. RESULTS CsA significantly inhibited the increase of RV systolic pressure and RVHI, compared with MCT group (P0.05 or P0.01). Histological examination revealed that CsA effectively prevented RV cardiomyocytes hypertrophy. The transmission electron microscope examination demonstrated that the swollen and misshapen mitochondria in RV cardiomyocytes induced by MCT was improved by CsA. CsA effectively reduced the PCNA expression in RV cardiomyocytes. The effect of high dose CsA was more significant (P0.01). CONCLUSION CsA (1 mg·kg-1,ig,bid) can improve the RV remodeling effectively in MCTtreated rats. The mechanism may be related to the reduction of RV systolic pressure and the inhibition of the cardiac hypertrophy.
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OBJECTIVE To explore the effect and the preliminary mechanism of cyclosporine A (CsA) on the right ventricle remodeling caused by monocrotaline (MCT). METHODS Thirty-six Sprague-Dawley male rats were randomly divided into normal control group,MCT group,low and high dose of CsA treatment group. Rats were given a single dose of MCT (50 mg·kg-1, sc) for inducing the right ventricle remodeling. CsA (0.33 and 1 mg·kg-1,bid,ig) was administered from day 14 to day 21 respectively. The right ventricle (RV) and the left ventricle with septum (LV+SEP) were weighed separately. RVHI was measured as RV/(LV+SEP). The histological examination of RV were executed by light microscope. The ultramicrostructure of the RV tissues was observed under the transmission electron microscope. Immunohistochemical analysis was performed on paraffin-embedded RV tissue using the anti-proliferating cell nuclear antigen (PCNA) primary antibodies. RESULTS CsA significantly inhibited the increase of RV systolic pressure and RVHI, compared with MCT group (P0.05 or P0.01). Histological examination revealed that CsA effectively prevented RV cardiomyocytes hypertrophy. The transmission electron microscope examination demonstrated that the swollen and misshapen mitochondria in RV cardiomyocytes induced by MCT was improved by CsA. CsA effectively reduced the PCNA expression in RV cardiomyocytes. The effect of high dose CsA was more significant (P0.01). CONCLUSION CsA (1 mg·kg-1,ig,bid) can improve the RV remodeling effectively in MCTtreated rats. The mechanism may be related to the reduction of RV systolic pressure and the inhibition of the cardiac hypertrophy.
Key concepts: Ventricle, Proliferating cell nuclear antigen, Muscle hypertrophy, Immunohistochemistry, Internal medicine, Medicine, Pathology, Endocrinology