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目的探讨心房颤动(房颤)患者心房肌组织中血管紧张素转换酶2(ACE2)的表达和血管紧张素转换酶抑制剂(ACEI)干预的影响及可能的信号传导途径。方法选取接受开胸手术的风湿性心脏病患者47例,手术中取右心耳处心房肌标本。采用 RT-PCR 法检测心房肌 ACE2和 ACEmRNA 水平,采用 Western blot 法检测 ACE、ACE2、细胞外信号调节激酶1/2(ERK1/2)和磷酸化的细胞外信号调节激酶1/2(pERK1/2)蛋白表达水平,应用放射免疫法检测心房肌组织血管紧张素Ⅱ(AngⅡ)水平。结果与窦性心律组相比,持续性房颤组心房肌组织中 ACE2表达显著减少(P<0.05),而 ACE 的表达和 AngⅡ含量显著增加(P<0.05)。ERK1/2的活化水平在持续性房颤组较窦性心律组明显增加(P<0.05)。与持续性房颤组相比,ACEI 干预组 ACE2表达水平显著增加(P<0.01),ERK1/2的活化水平显著降低(P<0.05),而 ACE 表达和 AngⅡ含量差异无统计学意义。结论房颤患者心房肌组织中 ACE2表达下调,ACE/ACE2平衡失调;ACEI 对房颤的长期临床效应可能与其上调 ACE2、抑制有丝分裂素激活蛋白激酶信号途径有关。
Objective To investigate the effects of angiotensin-converting enzyme 2 (ACE2) expression and angiotensin-converting enzyme inhibitor (ACEI) intervention on atrial fibrillation in patients with atrial fibrillation (AF) and possible signal transduction pathways. Methods Forty-seven patients with rheumatic heart disease undergoing thoracotomy were selected, and the atrial specimens were collected from the right atrial appendage. The levels of ACE2 and ACE mRNA in atrial myocardium were detected by RT-PCR. The expressions of ACE, ACE2, extracellular signal-regulated kinase 1/2 (ERK1 / 2) and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1 / 2) protein expression levels of atrial tissue using radioimmunoassay angiotensin Ⅱ (Ang Ⅱ) levels. Results Compared with sinus rhythm group, the expression of ACE2 in atrial fibrillation group was significantly decreased (P <0.05), while the expression of ACE and Ang Ⅱ content were significantly increased (P <0.05). The activation level of ERK1 / 2 in CAF group was significantly higher than that in sinus rhythm group (P <0.05). Compared with persistent AF group, the expression level of ACE2 in ACEI group was significantly increased (P <0.01), and the activation level of ERK1 / 2 was significantly decreased (P <0.05), but there was no significant difference between ACE expression and Ang Ⅱ content. Conclusions ACE2 expression is down-regulated and ACE / ACE2 is imbalanced in atrial fibrillation. The long-term clinical effect of ACEI on atrial fibrillation may be related to its up-regulation of ACE2 and inhibition of mitogen-activated protein kinase signaling pathway.