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作 者:秦晓毅[1,2] 卢新政[1] 张辉[1] 杨玉青[1] 杨晓慧[1] 郑宏健[1] 黄红娟[1] 孔祥清[1] 黄峻[1]
机构地区:[1]南京医科大学第一附属医院心内科,南京210029 [2]赣州市人民医院老年病科,江西赣州341000
出 处:《中国临床药理学杂志》2014年第1期11-13,共3页The Chinese Journal of Clinical Pharmacology
基 金:国家自然科学基金资助项目(30770890)
摘 要:目的观察佐芬普利对大鼠肥大心肌细胞ACE2和Mas受体的影响。方法原代培养大鼠心肌细胞,随机分为3组:正常组、模型组、实验组。模型组与实验组以去甲肾上腺素干预,致细胞肥大;48 h后,实验组加佐芬普利干预。RT-PCR法检测正常组、模型组的心肌细胞脑钠肽(BNP)mRNA水平及各组ACE2和Mas mRNA表达水平,Western blotting技术检测两者蛋白表达水平。结果去甲肾上腺素诱导48 h后,体外培养的心肌细胞BNP mRNA水平较正常组显著升高(P<0.01);与正常组相比,模型组心肌细胞ACE2和Mas mRNA及蛋白水平无明显变化(P>0.05)。实验组较模型组ACE2显著升高(P<0.01),Mas轻度升高(P<0.05)。讨论去甲肾上腺素成功诱导心肌细胞肥大,佐芬普利逆转心肌肥厚作用,可能与其上调心肌细胞ACE2和Mas受体表达有关。Objective To study the effect of reversal the hypertrophic cardiomyocytes and ACE2/angiotensin ( 1 - 7 )/Mas receptor axis in cel- lular level of zofenopril, which provides the theoretical basis with reversal of myocardial remodeling. Methods Cultivation of rat primary myocar- dial cells, intervened 48 hours by norepinephrine to make mast cells, then added with zofenopril to culture continue. Randomly divided into three groups with all cells:normal group, model group and experiment group. After 48 hours with norepinephrine, tested brain natriuretic pep- tide (BNP) mRNA between normal group and model group by RT- PCR. Detected mRNA levels of ACE2 and Mas of each group by RT - PCR, and tested the protein expressions of ACE2 and Mas receptor by western blotting. Results BNP mRNA level of myocardial cells signifi- cantly increased (P 〈 0. 01 ) after 48 hours with norepinephrine com- pared with normal group. Compared with normal group, ACE2 and Mas receptor mRNA and protein expression without obvious changes (P 〉 0. 05) in model group; compared with model group, ACE2 mRNA and protein expression were remarkable increased ( P 〈 0. 01 ) in experiment group, Mas mRNA and protein expression increased mildly (P 〈 0. 05 ). Conclusion We can establish hypertrophic cardiomyocyte model suc- cessfully by norepinephrine. The zofenopril up- regulate ACE2 and Mas may have relationship with reversal of myocardial remodeling, provide new therapeutic targets for myocardial hypertrophy.
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