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作 者:李成海[1] 张聪恪[1] 赵静[2] 许泼实[2] 邹国林[3]
机构地区:[1]河南省疾病预防控制中心,郑州450083 [2]河南省人民医院中心实验室 [3]武汉大学生命科学学院
出 处:《中原医刊》2006年第19期1-3,共3页Central Plains Medical Journal
基 金:国家自然科学基金资助项目(30370366)
摘 要:目的探讨狼疮性肝病患者活性氧和线粒体膜超极化与组织损伤的关系。方法使用荧光探针对26例血清抗线粒体抗体阳性的狼疮性肝病患者外周血淋巴细胞活性氧和线粒体膜电位的检测分析,同时选择20例狼疮患者做对照。结果抗线粒体抗体阳性的狼疮性肝病患者活性氧水平比狼疮患者高(P<0.01);线粒体膜电位极化与活性氧水平一致。结论早期线粒体膜超极化和/或活性氧触发淋巴细胞凋亡可能是导致系统性红斑狼疮(SLE)性肝病患者病理损伤的机制之一。Objective To establish whether the disease feature correlates with production of reactive oxygen intermediates (ROI) and mitochondrial hyperpolarization in peripheral blood lymphocytes (PBL) from patients with liver involvement in systemic lupus erythematosus (SLE). Methods Twenty-six anti-mitochondrial antibodies (AMA) positive SLE patients with liver involvement and 20 randomly selected patients with SLE alone as a matched case control were enrolled into the study. ROI and mitochondrial transmembrane potential (△ψm) were detected by the immunofluoreseent probe using the flow cytometry. Results Compared with the 20 individuals with SLE, we found that both the △ψm and ROI in PBL were elevated in the 26 AMA-positive SLE patients. Conclusion Mitochondrial hyperpolarization is a likely cause of increased ROI production and the both may be ultimately responsible for cell apoptosis in AMA-positive patients with liver involvement in SLE.
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