抗坏血酸诱导实验动物淀粉样变性的消退。
Ascorbic acid-induced regression of amyloidosis in experimental animals.
作者信息
Ravid M, Chen B, Bernheim J, Kedar I
出版信息
Br J Exp Pathol. 1985 Apr;66(2):137-41.
Ascorbic acid was found to accelerate amyloid degradation in an experimental animal model. Based on experiments in vitro which demonstrated the ability of ascorbic acid to restore the amyloid-degrading activity of amyloidotic human serum, the effect of orally administered ascorbic acid was tested in casein-induced murine amyloidosis. Histopathological examination of splenic tissue of mice killed at different times after the termination of the amyloidogenic stimulus showed a markedly decreased amyloid deposition in ascorbic acid-treated animals as compared to the controls. The effect of ascorbic acid was to a certain degree dose-dependent. Colchicine blocked amyloid synthesis when administered during amyloid induction. In animals which were given the drug during the post-induction period it had no effect. The amyloid-degrading activity of mouse serum was reduced in amyloidotic mice. Administration of ascorbic acid partially restored the amyloid-degrading activity of these animals.
在一个实验动物模型中发现，抗坏血酸可加速淀粉样蛋白的降解。基于体外实验表明抗坏血酸能够恢复淀粉样变性人血清的淀粉样蛋白降解活性，于是在酪蛋白诱导的小鼠淀粉样变性模型中测试了口服抗坏血酸的效果。对在淀粉样蛋白生成刺激终止后不同时间处死的小鼠脾脏组织进行组织病理学检查发现，与对照组相比，抗坏血酸处理的动物中淀粉样蛋白沉积明显减少。抗坏血酸的作用在一定程度上呈剂量依赖性。秋水仙碱在淀粉样蛋白诱导期间给药时可阻断淀粉样蛋白合成。在诱导后阶段给药的动物中，秋水仙碱没有效果。淀粉样变性小鼠的小鼠血清淀粉样蛋白降解活性降低。给予抗坏血酸可部分恢复这些动物的淀粉样蛋白降解活性。
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