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目的:检测风湿性心脏病心房颤动患者心房组织中结缔组织生长因子(CTGF)、肝细胞生长因子(HGF)、MAPKs信号通路分子的磷酸化水平,探讨房颤心房纤维化的可能分子机制。方法:21例风湿性心脏病患者于术中获取约200 mg的右心房肌组织,分为窦律(SR)组11例和房颤(AF)组10例。Masson病理染色观察心房纤维化,免疫组化测定心房肌组织中CTGF、HGF的蛋白表达,western blot测定心房肌组织中MAPKs信号通路分子的磷酸化水平。结果:与SR组比较,CTGF、MAPKs信号通路分子的磷酸化水平及胶原容积分数在AF组显著增加,而HGF的蛋白表达量显著降低,差异具有统计学意义(P<0.001)。结论:风湿性心脏病房颤患者心肌组织中CT-GF的表达增加及HGF的表达降低,可能激活了MAPKs信号通路分子的磷酸化表达,从而促进心房纤维化,参与房颤的发生与维持。
Objective: To detect the phosphorylation of connective tissue growth factor (CTGF), hepatocyte growth factor (HGF) and MAPKs signaling molecules in atrial fibrillation patients with rheumatic heart disease and to explore the possible molecular mechanism of atrial fibrillation in atrial fibrillation. METHODS: Twenty-one patients with rheumatic heart disease received approximately 200 mg of right atrial muscle during surgery, and were divided into sinus rhythm (SR) group (n = 11) and AF group (n = 10). Masson staining was used to observe the atrial fibrosis. The expression of CTGF and HGF in atrial myocardium was detected by immunohistochemistry. The phosphorylation of MAPKs signal pathway in atrial myocardium was detected by western blot. Results: Compared with SR group, the phosphorylation of CTGF and MAPKs and collagen volume fraction increased significantly in AF group, while the expression of HGF protein was significantly decreased (P <0.001). Conclusion: The increased expression of CT-GF and the decreased expression of HGF in myocardium of patients with rheumatic heart disease may activate the phosphorylation of MAPKs signaling molecules, thereby promoting atrial fibrosis and participating in the occurrence and maintenance of atrial fibrillation.