Kelly R H, Rao K N, Harvey V S, Lombardi B
Digestion. 1981;22(1):1-7. doi: 10.1159/000198588.
Induction of acute hemorrhagic pancreatic necrosis by dietary means in mice produces alterations in the serum complement system. Total hemolytic complement, i.e., CH50, and native C3 levels fall during the development of pancreatitis while, at the same time, what could be immunoreactive C3 degradation products are demonstrable both in the circulation and in the urine. No evidence of renal deposition of C3 was obtained by immunofluorescence analysis, although marked alterations in proteinuria were observed, suggesting that renal dysfunction(s) is a feature of acute hemorrhagic pancreatic necrosis. Lack of renal complement deposition, together with our earlier negative findings with respect to pancreatic localization, suggests that serum complement alterations are side effects of the pancreatitis, attributable to intravascular, pancreatic enzyme-mediated degradation of serum complement components.
通过饮食方式诱导小鼠发生急性出血性胰腺坏死会导致血清补体系统发生改变。在胰腺炎发展过程中，总溶血补体即CH50以及天然C3水平下降，与此同时，循环系统和尿液中均可检测到具有免疫反应性的C3降解产物。尽管观察到蛋白尿有明显改变，但免疫荧光分析未发现C3在肾脏沉积的证据，这表明肾功能障碍是急性出血性胰腺坏死的一个特征。肾脏缺乏补体沉积，以及我们之前在胰腺定位方面的阴性结果，提示血清补体改变是胰腺炎的副作用，归因于血管内胰腺酶介导的血清补体成分降解。
