摘要
目的探讨阿托伐他汀体外抑制心肌肥厚的药理作用。方法体外培养新生大鼠的心室肌细胞,用血管紧张素Ⅱ(AngⅡ)诱导心肌细胞肥厚模型,以不同浓度的阿托伐他汀作用于心肌细胞,用软件分析测量心肌细胞表面积,3H-亮氨酸参入法检测心肌细胞蛋白合成速率及使用RT-PCR半定量测定心钠素(ANP),脑钠素(BNP)和特异分布于心脏的丝氨酸蛋白酶(Corin)的表达变化。结果AngⅡ可成功诱导体外培养的新生大鼠心室肌细胞肥大,表现为心肌细胞面积和3H-亮氨酸的参入增加,ANP、BNP、Corin表达升高等特征性改变,从而分析阿托伐他汀对心肌肥厚的作用。阿托伐他汀可逆转上述变化并呈剂量依赖性,而作为溶剂的DM-SO对肥大的心肌细胞差异无显著性。结论阿托伐他汀抑制AngⅡ介导的体外心肌细胞肥大,预示其具有降脂以外的其他重要药理作用。
Aim To investigate the effect of atorvasta- tin on Ang Ⅱ-induced hypertrophic myocytes in vitro.Methods Hypertrophy in neonatal rat cardiac myocytes （MC） was established via culture with angiotensin Ⅱ （Ang Ⅱ ）, then the effect of atorvastatin on the hypertrophy was detected. The surface area of MC was analyzed with the aid of NIH Image J software, and the synthetic rate of protein in MC was detected with ^3H- leucine incorporation, mRNA expression of atrial natriuretic peptide （ANP）, brain natriuretic peptide （BNP） and Corin was measured using reverse transcription-polymerase chain reaction （RT-PCR）. Re-suits The surface area, ^3H-leucine incorporation and mRNA expression of ANP, BNP and Corin in hypertrophic myocytes were decreased after treatment of atorvastatin in a dose-dependent manner, but no change was found in the myocytes treated with DMSO. Conclusion Atorvastatin inhibits cardiac hypertrophy in vitro and the role might be independent of the cholesterol lowering effect of atorvastatin.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2006年第1期23-27,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30270551)
