Sato M, Nakajima Y, Koshikawa S
Clin Nephrol. 1987 Mar;27(3):141-6.
Recently, we reported on an experimentally-induced model of IgA nephropathy in mice, in which the lesions were very similar to those found in human IgA nephropathy. This model was achieved by long-term oral immunization and intravenous injection of colloidal carbon in order to achieve reticuloendothelial (RES) dysfunction. In this paper, we investigated the effects of sodium cromoglycate (SCG), an anti-allergic agent, on this model. Mice were treated with a small amount of colloidal carbon three times to block the RES, in addition to receiving oral administration of lactalbumin, as a food antigen. Open renal biopsy was performed at 18 weeks after the RES blockade, and mice were divided into 2 groups. One group received orally administered SCG and lactalbumin [SCG(+)], and the other group received lactalbumin only [SCG(-)] from 19 to 30 weeks. At 30 weeks, all mice were sacrificed for histopathological observation of renal tissue and blood sampling. IgA nephropathy had developed in all mice of the SCG(-) group, but had not developed in 7 out of the 9 mice in the SCG(+) group, at 30 weeks. Serum IgA levels obtained on sacrifice were significantly higher in the SCG(-) group. It was concluded that SCG effectively inhibited, not only the onset, but also the progression of IgA nephropathy in our original model. The effective mechanisms of this drug may act to suppress the local immunity produced through sensitization of gastrointestinal mucosa by food antigens.
最近，我们报道了一种实验诱导的小鼠IgA肾病模型，其病变与人类IgA肾病中发现的病变非常相似。该模型是通过长期口服免疫和静脉注射胶体碳来实现网状内皮系统（RES）功能障碍而建立的。在本文中，我们研究了抗过敏药物色甘酸钠（SCG）对该模型的影响。除了口服乳白蛋白作为食物抗原外，小鼠还用少量胶体碳处理三次以阻断RES。在RES阻断后18周进行开放性肾活检，并将小鼠分为2组。一组从第19周到第30周口服SCG和乳白蛋白[SCG(+)]，另一组仅口服乳白蛋白[SCG(-)]。在第30周时，处死所有小鼠以进行肾组织的组织病理学观察和采血。在第30周时，SCG(-)组的所有小鼠均发生了IgA肾病，但SCG(+)组的9只小鼠中有7只未发生。处死时获得的血清IgA水平在SCG(-)组中显著更高。得出的结论是，在我们最初的模型中，SCG不仅有效地抑制了IgA肾病的发生，而且抑制了其进展。该药物的有效机制可能是通过抑制食物抗原对胃肠道黏膜致敏产生的局部免疫反应来发挥作用。
