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机构地区:[1]哈尔滨医科大学附属第二医院,黑龙江哈尔滨150086 [2]哈尔滨理工大学医院
出 处:《心血管康复医学杂志》2010年第4期346-349,358,F0004,共6页Chinese Journal of Cardiovascular Rehabilitation Medicine
基 金:黑龙江省青年基金QC06C053;哈尔滨医科大学附属第二医院青年启动基金QN2007-07;黑龙江省卫生厅课题2006-141;省部共建黑龙江省教育部心肌缺血机理与诊疗技术重点实验室
摘 要:目的:研究心肌营养素-1(CT-1)对血管紧张素Ⅱ(AngⅡ)诱导的心肌细胞肥大的影响.方法:利用AngⅡ刺激心肌细胞,导致细胞肥大,应用CT-1反义脱氧寡核苷酸进行干预.检测心肌细胞大小及3H-亮氨酸掺入率的变化;以逆转录聚合酶链反应(RT-PCR)检测CT-1 mRNA及β-肌球蛋白重链(β-MHC) mRNA表达,免疫组织化学法检测心肌细胞CT-1蛋白的表达. 结果:经AngⅡ刺激后,在相差显微镜下可见心肌细胞面积变大,3H-亮氨酸掺入率、CT-1蛋白的表达增高;CT-1和β-MHC mRNA水平的表达增加.利用Fugene 6 可将CT-1反义脱氧寡核苷酸转染入心肌细胞.CT-1反义脱氧寡核苷酸组心肌细胞面积较肥大组明显减小[(81.257±3.995)mm2∶( 127.214±5.693) mm2],3H-亮氨酸掺入量[(1653.33±17.91)cpm∶(1971.50±42.16) cpm]及CT-1蛋白[(3.16±0.17) %∶(3.51±0.29)%]明显减少;CT-1[(0.2137±0.0227)∶(0.4023±0.0160)]和β-MHC mRNA[(0.5032±0.0261)∶(0.773 4±0.0486)]表达亦显著减少(P〈0.05-〈0.01).各指标Fugene 6组、错义组与肥大组无明显差异.结论:AngⅡ致心肌细胞肥大过程中伴有CT-1表达增加,应用CT-1反义脱氧寡核苷酸后可使之下降,说明CT-1参与了心肌细胞的肥大机制.Objective: To study the effect of cardiotrophin- 1 (CT-1) on hypertrophy of cardiocytes induced by angiotensin Ⅱ (Ang Ⅱ ). Methods: The cultured cardiocytes were treated with AngⅡ to induce hypertrophy and given with CT-1 antisense oligodeoxyribonucleotide (ASODN). The cell size and 3H-leucine incorporation were examined. The mRNA levels of CT-1 and β-myosin heavy chain (β-MHC) were examined by real-time PCR method. The protein expressions of CT- 1 were examined by immunohistochemistry method. Results : Stimulated by Ang It , the cardiocytes were enlarged under the contrast phase microscope. After stimulated by Ang Ⅱ , 3H- leucine incorporation and the protein expression of CT- 1 increased in the hypertrophic cardiocytes. The mRNA levels of CT- 1 and 3- MHC increased also. Compared with hypertrophy group, the area of cardiocytes [- ( 127. 214±5. 693) mm^2 vs. (81. 257±3. 995) mm^2], 3H-leueine incorporation [ (1971.50±42.16) cpm vs. (1653.33± 17.91) epm], protein expression of CT-1 [(3.51±0. 29)% vs. (3.16±0.17) %], CT-1 mRNA [ (0. 4023±0. 0160) vs. (0. 2137±0. 0227)] and β-MHC mRNA [- (0. 773 4±0. 0486) vs. (0. 5032±0. 0261)1 significantly decreased in CT-1 ASODN group (given by CT- 1 ASODN), P〈0.05 - 〈0.01. These indexes were no significantly difference among CT- 1 MSODN (missence oligodeoxyrihonucleotide) group, hypertrophy group and Fugene 6 group. Conelusiom Ang Ⅱmay induced the cardiocytes hypertrophy. The expression of CT-1 increased in hypertrophic cardiocytes stimulated by Ang Ⅱ. The CT- 1 ASODN inhibited the increased expression of CT- 1 in hypertrophic cardiocytes stimulated by Ang Ⅱ.
分 类 号:R541.75[医药卫生—心血管疾病]
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