| 熊果酸抑制AngⅡ诱导大鼠心肌细胞肥大实验研究 |
| 投稿时间：2016-04-13 修订日期：2016-04-22 点此下载全文 |
| 引用本文：裴菱花,夏勇.熊果酸抑制AngⅡ诱导大鼠心肌细胞肥大实验研究[J].医学研究杂志,2016,45(11):90-94 |
| DOI：
10.11969/j.issn.1673-548X.2016.11.023 |
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| 中文摘要:目的 探讨熊果酸（ursolic acid，UA）对血管紧张素Ⅱ（angiotensin Ⅱ，AngⅡ）诱导大鼠心肌细胞肥大的抑制作用及其可能机制。方法 按常规方法分离并培养新生大鼠心肌细胞。CCK-8法确定UA（2、4、8、16μmol/L）对心肌细胞的最佳作用浓度，利用AngⅡ诱导建立新生大鼠心肌细胞肥大模型。实验分对照组（control组）、AngⅡ组、UA干预组、LY294002（PI3K/Akt通路抑制剂）干预组共4组。UA和LY294002均预处理心肌细胞30min。以心肌细胞表面积、β-肌球蛋白重链（β-MHC）mRNA和脑钠肽（BNP）mRNA表达作为心肌细胞肥大标志，同时使用蛋白免疫印迹法检测T-Akt（total Akt）和p-Akt（phospho-Akt）蛋白表达。结果 显微镜下观察各组心肌细胞生长良好。与control组相比，AngⅡ组和UA干预组大鼠心肌细胞表面积增加（P<0.05），LY294002干预组心肌细胞表面积差异无统计学意义（P>0.05）；与AngⅡ组相比，UA干预组和LY294002干预组大鼠心肌细胞表面积减小（P<0.05）。与control组相比，AngⅡ组的p-Akt蛋白、BNP mRNA和β-MHC mRNA表达显著增加（P<0.05）；与AngⅡ组相比，UA干预组和LY294002干预组的p-Akt蛋白、BNP mRNA和β-MHC mRNA表达均降低（P<0.05）；UA干预组和LY294002干预组之间p-Akt蛋白、BNP mRNA和β-MHC mRNA表达均差异无统计学意义（P>0.05）；4个实验组间T-Akt蛋白水平差异无统计学意义（P>0.05）。结论 （1）AngⅡ诱导的新生大鼠心肌细胞肥大模型中，心肌细胞表面积增加，BNP mRNA和β-MHC mRNA表达升高，同时伴有p-Akt蛋白表达增加，提示PI3K/Akt通路在AngⅡ致心肌细胞肥大中起重要作用。（2）UA能减轻AngⅡ诱导的大鼠心肌细胞肥大，使心肌细胞表面积减小，p-Akt蛋白、BNP mRNA和β-MHC mRNA表达减少，这与LY294002作用一致，提示UA可能是通过抑制PI3K/Akt通路而发挥抗心肌肥大作用。 |
| 中文关键词:熊果酸 心肌细胞肥大 AngⅡ LY294002 |
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| Study of the Inhibiting Effect of Ursolic Acid on Cardiocytes Hypertrophy in Rats Induced by AngⅡ |
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| Abstract:Objective To explore the inhibitory effect of ursolic acid on the hypertrophy of cardiac myocytes induced by angiotensin Ⅱ (AngⅡ) in rats and its possible mechanism. Methods Neonatal rat cardiomyocytes were isolated and cultured by conventional method. The optimal concentration of UA (2, 4, 8, 16μmol/L) on cardiomyocytes was determined using CCK-8 colorimetric method.Hypertrophy model of rat cardiomyocytes was set up by adding AngⅡ. The experiment was divided into four groups:control group,AngⅡ group,UA intervention group,LY294002(PI3K/Akt inhibitor) intervention group. Cardiomyocytes were pretreated with UA or LY294002 for 30 minutes. Myocardial cell area and beta myosin heavy chain (β-MHC)mRNA as well as brain natriuretic peptide(BNP)mRNA were regarded as the marker of cardiomyocytes hypertrophy. Western blot was used to detect expression of T-Akt and p-Akt protein. Results The cells grew well under the phase contrast microscope. Compared with the control group, AngⅡ intervention group and UA group increased cell surface area (P<0.05),then LY294002 intervention group had no significant difference in cell surface area (P>0.05). Compared with AngⅡ group, UA group and LY294002 intervention group reduced surface area of myocardial cells(P<0.05). Compared with the control group, AngⅡ significantly increased the expression of p-Akt protein as well as BNP mRNA and β-MHC mRNA (P<0.05). Compared with the AngⅡ group, LY294002 group and UA group could significantly reduce them(P<0.05). There was no significant difference in the level of above indexes between LY294002 group and UA group (P>0.05). There was no significant difference in the level of T-Akt protein among the four experiment groups(P>0.05). Conclusion AngⅡ induced cardiomyocyte hypertrophy. UA significantly reduced the augmented myocardial cell surface area induced by AngⅡ and reduced the BNP mRNA and β-MHC mRNA level, as well as decreased p-Akt protein expression.It suggested that UA played the role of anti myocardial hypertrophy through inhibiting of the PI3K-Akt pathway. |
| keywords:Ursolic acid Cardiocyte hypertrophy AngⅡ LY294002 |
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