慢性心房颤动患者右心耳IL-1β、IL-6和肿瘤坏死因子-α基因表达的研究

Experimental Research on the Change of Gene Expression of Interleukin-1β, Interleukin-6 and Tumor Necrosis Factor-α in Right Atrial ppendages of Patients with Chronical Atrial Fibrillation

目的 观察慢性心房颤动(房颤)患者右心耳白介素-1β(IL -1β)、白介素- 6(IL -6)和肿瘤坏死因子-α(TNF α)基因表达的改变。方法 将术中获取的48例风湿性瓣膜病患者的右心耳分为2组,其中窦性心律组27 例,慢性房颤组21 例,以GAPDH为内参照基因,采用逆转录聚合酶链反应(RT- PCR)技术测定心房组织中IL -1β、IL- 6和TNF -α的mRNA含量,用病理学检查评价心房组织纤维化程度,用免疫组织化学检查评价IL- 1β和TNF- α的表达情况。结果 与窦性心律组相比,慢性房颤组IL- 1β、IL- 6和TNF -α的mRNA表达显著增加。慢性房颤患者心房组织有显著的纤维化,而且心房肌细胞IL- 1β和TNF -α的表达强度也显著大于窦性心律组。结论 慢性房颤患者心房组织IL- 1β、IL -6和TNF- α的mRNA表达显著增加,炎症反应可能是房颤发生和维持的因素之一。

Objective To investigate whether the gene expression of interleukin-1β(IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) in right atrial appendage is altered in patients with chronic atrial fibrillation. Methods 48 patients with rheumatic heart disease were enrolled. Twenty-seven patients had no history of atrial fibrillation, and twenty-one patients had atrial fibrillation. Atrial tissue was obtained from the right atrial appendage during open heart surgery. The mRNA expression of IL-1β, IL-6 and TNF-α was measured by reverse transcription-polymerase chain reaction (RT-PCR). The protein expression of IL-1β and TNF-α was detected by immunhistochemical method. The fibrosis of right atrial appendage was detected by Masson staining. Results The expression of IL-1β/GAPDH, IL-6/GAPDH and TNF-α/GAPDH was significantly increased in patients with chronic atrial fibrillation compared with patients with sinus rhythm (1.48±0.38 vs 0.78±0.27, P<0.001; 1.46±0.48 vs 0.73±0.25, P<0.001; 1.71±0.98 vs 0.73±0.29, P< 0.001). The fibrosis of right atrial appendage was significantly increased in patients with chronic atrial fibrillation. The protein expression of IL-1β and TNF-α was significantly increased in patients with chronic atrial fibrillation. Conclusion The mRNA expression of IL-1β, IL-6 and TNF-α is significantly increased in patients with chronic atrial fibrillation, inflammation may be one of mechanisms for the development and maintainance of atrial fibrillation.