活化补体诱生一氧化氮介导肝细胞损伤的实验研究

目的：探讨活化本补体在大鼠枯否细胞（KC）分泌一氧化氮（NO）的影响及其与肝细胞损伤关系。方法：大鼠KC＋肝细胞（HC）联合培养分别与酵母多糖活化人血清（ZAHS），抗人C3、C3中和ZAHS以及ZAHS＋氨基胍（iNOS抑制剂）作用后，观察培养上清中不同时相点的NO和乳酸脱氢酶（LDH）。结果：ZAHS作用组KC＋HC联合培养的上清中NO和LDH各时相点的测值显著升高，P＜0．01；中和血清组和氨基胍组培养上清中NO分别下降53．4％－62．8％和68．1％－72．1％，LDH分别下降56．0％－66．5％和51．2％－57．2％，与作用组相差显著，P＜0．01。结论：ZAHS中的C3、C5片断可激发KC生成NO，介导肝细胞损伤，这可能是某些病理情况下本介导肝损伤的机制之一。

EXPERIMENT OF NITRIC OXIDE INDUCED BY ACTIVATED COMPLEMENTS MEDIATING HEPATOCYTE INJURY

Objective: To investigate whether the activated complements can induce Kupffer cell (KC) to secrete nitric oxide (NO) and its role in hepatocyte (HC) injury.Method: Pre-treated with zymosan-activated human serum (ZAHS), or ZAHS neutralized by anti-C 3,and C 5 serum, or ZAHS and aminoguanidine (AGD), KC/HC were co cultured. The levels of NO and lactate dehydrogenatase (LDH) in supernatant were measured at different times. Result: At each designed time, the levels of NO and LDH in ZAHS treated group increased significantly than in the normal (p<0.01). But in neutralized ZAHS treated and ZAHS+AGD treated group, the levels decreased sharply (p<0.01), and the level of NO reduced to 53.4%-62.8% and 68.1%-72 1%,respectively, and the level of LDH did to 56 0%-66 5% and 51 2%-57 2%, respectively. There was a significant correlation between NO and LDH (r=0.9528). Conclusion: The fragments of C 3 and C 5 in ZAHS can stimulate KC to secrete NO, by which they can mediate hepatocyte injury, which maybe the potential mechanism of liver injury mediated by complements in some pathological condition.