补体灭活对氯化汞诱导的棕色挪威大鼠肾小球肾炎的影响。
Effects of decomplementation on mercuric chloride-induced glomerulonephritis in Brown-Norway rats.
作者信息
Capron M, Bascou C, Vial M C, Grossetete J, Hinglais N, Girard J F, Druet P
出版信息
Clin Exp Immunol. 1982 Sep;49(3):611-7.
The course of mercuric chloride-induced immune glomerulonephritis is characterized by complement activation, intensive proteinuria, linear and then granular IgG and C3 deposits in the glomeruli. To assess the role of complement activation in the occurrence of the disease, decomplementation was achieved by intravenous injections of cobra venom factor in rats injected with mercuric chloride. In these animals, proteinuria still appeared while rats were decomplemented by cobra venom factor through the alternative pathway. These rats exhibited linear IgG deposits without detectable C3 deposits. In the rats injected with cobra venom factor alone, no proteinuria, no classical pathway complement activation and no renal IgG or C3 deposits were observed. Therefore, in Brown-Norway rats intoxicated with mercuric chloride, proteinuria appears to be at least in part complement independent.
氯化汞诱导的免疫性肾小球肾炎病程的特征为补体激活、大量蛋白尿、肾小球内先出现线性而后为颗粒状的IgG和C3沉积。为评估补体激活在该疾病发生中的作用，通过给注射了氯化汞的大鼠静脉注射眼镜蛇毒因子来实现补体灭活。在这些动物中，当大鼠通过替代途径被眼镜蛇毒因子灭活补体时，蛋白尿仍会出现。这些大鼠呈现线性IgG沉积，未检测到C3沉积。在仅注射眼镜蛇毒因子的大鼠中，未观察到蛋白尿、经典途径补体激活以及肾脏IgG或C3沉积。因此，在氯化汞中毒的棕色挪威大鼠中，蛋白尿似乎至少部分独立于补体。
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