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作 者:肖骅[1] 雷寒[1] 王曦[1] 胥雪莲[1] 游小均[1]
机构地区:[1]重庆医科大学附属第一医院心血管内科,重庆400016
出 处:《第三军医大学学报》2008年第12期1193-1196,共4页Journal of Third Military Medical University
基 金:重庆市卫生局项目(2007-2-041)~~
摘 要:目的观察转化生长因子β1(TGF-β1)在风湿性心脏病(风心病)心房颤动(房颤)患者心房组织中的表达情况,探讨其在风心病房颤心房纤维化中的作用及意义。方法38例风心病接受换瓣手术者于术中获取的右心耳分为3组,其中窦性心律组8例,阵发性房颤组10例,持续性房颤组20例。对各组心房组织,应用羟脯氨酸含量测定法及Mas-son染色检测胶原含量及分布;应用免疫组化技术检测TGF-β1蛋白表达及分布;应用RT-PCR检测TGF-β1 mRNA水平,应用Western blot检测TGF-β1的蛋白表达。结果TGF-β1主要表达在心肌细胞的细胞质;与风心病窦性心律组相比,TGF-β1的mRNA和蛋白表达及胶原含量在阵发性房颤组(P<0.05)和持续性房颤组均显著增加(P<0.01);与阵发性房颤组相比,持续性房颤组中TGF-β1 mRNA和蛋白表达及胶原含量继续明显增加(P<0.05)。相关分析发现TGF-β1的mRNA、蛋白表达程度与心房胶原含量均呈正相关(r=0.37,P<0.05;r=0.45,P<0.01)。结论风心病患者心房组织中TGF-β1的mRNA和蛋白表达上调可能是心房纤维化发生的分子机制之一,在风心病房颤的发生和维持中起一定的作用。Objective To investigate the role of TGF-β1 in the atrial myocardial fibrosis in the patient with rheumatic heart disease(RHD). Methods Of 38 RHD patients, 8 were with sinus rhythm, 10 with paroxysm atrial fibrillation (pAF) and 20 with chronic AF(cAF) ( ≥6 months). The right atrial muscle specimens were obtained during the operation on mitral valve replacement. The collagen content and distribution of myocardium specimens were obtained by hydroxyproline detection and Masson staining. Expression and distribution of TGF-β1 were examined by immunohistochemical staining. The mRNA content of TGF-β1 was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Proteins of TGF-β1 was measured by Western blotting. Results RHD atrial myocardium had high content of collagen. TGF-β1 was distributed mainly in myocardium cells. Both of the collagen content and mRNA or protein expression of TGF-β1 in pAF group (P 〈0. 05) and cAF group (P 〈0. 01 ) was stronger than that in sinus rhythm group; cAF group was stronger than that in pAF group (P 〈 0. 05 ). The mRNA and protein expression of TGF-β1 in RHD was increased and correlated positively with the content of myocardial collagen. Conclusion The mRNA and protein expression of TGF-β1 in human atria may have correlation with the initiation or maintenance of AF, and contribute for the development of atrial fibrosis in patients with RHD, which produces a structural basis for AF.
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