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实验性肾小球肾炎时,由浸润白细胞产生的活性氧,对肾小球损害起重要作用,已经下述实验证实:①应用实验肾炎模型马杉肾炎(抗肾小球基底膜抗体所致),投给肾小球上聚集白细胞的大白鼠,以白细胞活化因子佛波醇肉豆蔻酸盐乙酸盐(phorbolmyristate acetate,PMA),可增强活性氧产生,引起明显肾小球内血栓形成;②从浸润肾小球内的白细胞释放的髓过氧化物酶(MPO)为正电荷酶,故与带负电荷的肾小球血管壁结合,接着与过氧化氢(H_2O_2)和氯离子反应,生成次氯酸(OC(?))以及单线态氧((?)O_2),进一步引起严重的组织损害。
Experimental glomerulonephritis, the active oxygen generated by infiltrating leukocytes play an important role in glomerular damage has been confirmed by the following experiments: (1) experimental nephritis model of bursin nephritis (anti-glomerular basement membrane antibody) , To rats with glomerular accumulation of leukocytes, and phorbol myristate acetate (PMA), a leukocyte activating factor, can enhance the production of reactive oxygen species and cause obvious glomerular thrombosis; Myeloperoxidase (MPO), released from white blood cells infiltrating the glomerulus, is a positively charged enzyme that binds to negatively charged glomerular wall and then reacts with hydrogen peroxide (H 2 O 2) and chloride ions to form Hypochlorous acid (OC (?)) And singlet oxygen (? O 2), further cause serious tissue damage.