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作 者:陈爱兰[1] 陈敏生[2] 何兆初[1] 刘启才[3] 董颀[4]
机构地区:[1]广州医学院第一附属医院心内科,510120 [2]广州医学院第二附属医院心内科 [3]广州医学院医学研究中心 [4]广州医学院生理教研室
出 处:《现代临床医学生物工程学杂志》2006年第6期475-477,共3页Journal of Modern Clinical Medical Bioengineering
基 金:国家自然科学基金(30440053)
摘 要:目的观察伊贝沙坦对血管紧张素Ⅱ(AngⅡ)所致心肌细胞中蛋白质合成速率及肌球蛋白重链(MHC)基因表达改变的影响。方法以AngⅡ及伊贝沙坦分别或同时作用于培养的细胞。采用放射性同位素[3H]-leu掺入法检测培养心肌细胞蛋白质合成速率。应用荧光定量PCR方法检测心肌细胞心房利钠肽因子(ANF)以及α-MHC、β-MHC的表达。结果AngⅡ处理使心肌细胞中[3H]-Leu掺入增加(P<0.05),同时ANF mRNA的表达明显高于正常(P<0.05);α-MHC mRNA的表达显著低于正常(P<0.05),而β-MHC mRNA的表达显著高于正常(P<0.05),α-MHC/β-MHC的比值下降(P<0.05)。当伊贝沙坦与AngⅡ共同作用于培养的心肌细胞时,与AngⅡ组比较,[3H]-Leu的掺入明显下降(P<0.05),与正常组比无统计学意义(P>0.05);同时ANF的表达下降,与正常组比无统计学意义(P>0.05);心肌细胞中α-MHC的表达明显增高(P<0.05),而β-MHC mRNA的表达显著降低(P<0.05),α-MHC/β-MHC的比值上升(P<0.05)。结论伊贝沙坦能抑制AngⅡ所致的心肌细胞肥大和细胞中α-MHC向β-MHC表达的转换。Objective To investigate the effect of irbesartan on cardiac hypertrophy and myosin heary chain (MHC) gene expression induced by angiotensin Ⅱ (Ang Ⅱ )in rats. Methods Cardiocytes of neonatal SD were cultured with Ang Ⅱ. Irbesartan was used to inhibit the effect of Ang Ⅱ. For assessing protein synthesis rate, ANF, β-MHC and α-MHC gene expression in cardiomyocyte, the methods of ^3H- Leucine incorporation and RT-QT-PCR were used. Results Ang Ⅱ could significantly increase ^3H -Leucine incorporation and the gene expression of ANF and β-MHC compared with control group (P 〈 0. 05, 0. 05, 0. 05 ), but decrease α-MHC gene expression ( P 〈 0. 05 ), accompanied the decrease of α-MHC/β-MHC value(P 〈0.05 ). The effects of Ang Ⅱ were inhibited by irbesartan. The ^3H -Leucine incorporation and the gene expression of ANF and β-MHC were decreased in the co-stimulation with Ang Ⅱ and irbesartan, and no significant differences were found as compared with control group ( P 〉 0.05, 0. 05, 0. 05 ), but the gene expression of α-MHC was significantly inhanced ( P 〈 0. 05 ). Similarly the value of α-MHC/β-MHC was increased (P 〈 0. 05 ). Conclusion In cultured neonatal cardiocytes, irbesartan can inhibit cardiocyte hypertrophy and the shift from α-MHC to β-MHC gene expression induced by AngⅡ.
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