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目的探讨心房颤动(简称房颤)患者心房肌电和结构重构以及心功能下降的分子生物学机制。方法采集风湿性心脏瓣膜病(简称风心病)窦性心律患者12例(窦律组)和房颤患者16例(房颤组)的右心耳组织,应用半定量逆转录-聚合酶链反应方法,测定心房肌钙转运调控蛋白和钙激活中性蛋白酶(calpain1)的mRNA表达水平。结果与窦律组比较,房颤组L-型电压依赖钙通道a1c亚基(LVDCCa1c)、肌浆网Ca2+-ATP酶、兰尼碱受体的mRNA表达水平显著下调(P均<0.01),三磷酸肌醇受体的mRNA表达水平上调(P<0.05);房颤组心房肌cal-pain1的mRNA表达水平上调(P<0.05),且与LVDCCa1c的mRNA表达呈负相关(r=-0.583,P=0.019)。结论房颤患者心房肌钙转运调控蛋白和calpain1转录水平调控失衡可能是心房肌电和结构重构以及心功能下降的分2子生物学机制之一。
Objective To investigate the molecular mechanism of atrial fibrillation (atrial fibrillation) atrial myoelectricity and structural remodeling and cardiac function decline. Methods 12 cases of sinus rhythm (sinus rhythm group) and 16 cases of atrial fibrillation (right atrial appendage) of right atrial appendage were collected from patients with rheumatic heart valvular disease (rheumatic heart disease). Semi-quantitative reverse transcription-polymerase chain reaction The mRNA expression of calmodulin, atrial calcium transporter and calpain1, was measured. Results Compared with sinus rhythm group, the mRNA expression of L-type voltage-dependent calcium channel a1c subunit (LVDCCa1c), sarcoplasmic reticulum Ca2 + -ATPase and ryanodine receptor were significantly decreased in atrial fibrillation group (all P <0.01) (P <0.05). The mRNA expression of atrial cal-pain1 in atrial fibrillation group was up-regulated (P <0.05), and negatively correlated with the mRNA expression of LVDCCa1c (r = -0.583 , P = 0.019). Conclusion The unbalanced regulation of atrial calcium transport regulatory protein and calpain1 transcription in atrial fibrillation patients may be one of the sub-2 biological mechanisms of atrial fibrillation and structural remodeling and cardiac function decline.