Résumé
Objective:To explore the effect of endothelin-1 on atrial ifbrosis in patients with atrial ifbrillation (AF). Methods: A total of 72 patients with thoracotomy were studied, the patients were divided into 2 groups:AF group, n=39 and Sinus rhythm (SR) group, n=33. The mRNA and protein expressions of endothelin-1 (ET-1), platelet derived growth factor-B (PDGF-B) and collagen I (COL1) in right atrial appendage (RAA) tissue were measured by RT-PCR and Western blot analysis;meanwhile, the impact of ET-1 stimulation and non-selective ET-1 receptor antagonist (sulfafurazole SIZ) on PDGF-B mRNA and protein expressions in H9c2 cells were measured. Results: ①The RAA tissue mRNA and protein expressions in AF group were higher than those in SR group, as for ET-1 (2.830 ± 2.276) vs (1.220 ± 0.887) and (0.835 ± 0.241) vs (0.286 ± 0.083), both P Conclusion: ET-1 plays an important role in AF occurrence which might be related to PDGF-B regulation.
Résumé
Objective: To explore the relationship between atrial MMP-9 with its inhibitor (TIMP-1), anti-apoptosis gene (BCL-2) with apoptosis gene (BAX) and the aging with atrial remodeling in experimental dog model during atrial ifbrillation (AF), in order to better deal with the aging caused AF. Methods: The experimental dogs were divided into 4 groups: ①Adult with sinus rhythm (ASR) group, ②Elder with sinus rhythm (ESR) group and③Adult with AF (AAF) group,④Elder with AF (EAF) group. n=7 in each group. Chronic AF model was induced by rapid and persistent atrial pacing. The mRNA and protein expressions of MMP-9, TIMP-1 and BCL-2, BAX were measured by real time quantitative RT-PCR and Western blot analysis. The cellular ultra structural remodeling was examined by optical/electron microscopy, and the apoptosis index was determined by TUNEL method, Results: Compared with adult dogs, the elder dogs showed obviously increased expressions of MMP-9, BAX, and decreased expressions of TIMP-1, BCL-2, all P of MMP-9, BAX, all P Conclusion: The abnormal expressions of MMP-9/TIMP-1 and BCL-2/BAX might be one of the molecular mechanisms for aging caused AF in experimental dog model.