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通过化学修饰和活性亚片段对人血清IgG进行药理学激活的研究。II. 人血清IgG的羧酰胺甲基化轻链对各种溃疡模型的抑制作用及其抑制机制。

Studies on pharmacological activation of human serum IgG by chemical modification and active subfragments. II. Inhibitory effects of carboxamide-methylated L chain from human serum IgG on various ulcer models and its inhibition mechanism.

作者信息

Mimura T, Iwai M, Terada T, Kohda I, Tsujikawa K, Maeda K, Aonuma S

出版信息

J Pharmacobiodyn. 1983 Jul;6(7):449-58. doi: 10.1248/bpb1978.6.449.

DOI:10.1248/bpb1978.6.449
PMID:6417314
Abstract

In view of the strong inhibitory effects of the carboxamide-methylated L chain (Fr. I-L) from human IgG on gastric ulceration and juice secretion, we carried out various experiments to clarify the mechanism of its action and obtained the following results. Fr. I-L inhibited the gastric ulceration induced by phenylbutazone or aspirin in rats, but no appreciable effect was observed on stress or acetic acid ulceration. The distribution of 14C-labelled Fr. I-L increased particularly in the stomach mucous membrane of rats after the intravenous or intraperitoneal administration. The hexosamine content in the gastric mucous membrane, reduced by the treatment with phenylbutazone, aspirin or pylorus-ligation, was recovered by the administration of Fr. I-L to an intact level. The high total of hexosamine levels found in the gastric juice after aspirin treatment or pylorus-ligation were decreased by the injection of Fr. I-L or cimetidine. The histochemical observation revealed that the concomitant administration of Fr. I-L with phenylbutazone or aspirin prevented the abolishment of Hematoxylin-Eosin, Periodic Acid Schiff and Alcian Blue staining polysaccharides from the stomach epithelial cells.

摘要

鉴于人IgG的羧酰胺甲基化轻链(Fr.I-L)对胃溃疡形成和胃液分泌具有强烈的抑制作用,我们开展了各种实验以阐明其作用机制,并获得了以下结果。Fr.I-L抑制了大鼠中由保泰松或阿司匹林诱导的胃溃疡形成,但对应激性或乙酸诱导的溃疡形成未观察到明显影响。静脉内或腹腔内给药后,14C标记的Fr.I-L在大鼠胃黏膜中的分布尤其增加。保泰松、阿司匹林或幽门结扎处理使胃黏膜中的己糖胺含量降低,而给予Fr.I-L可将其恢复至正常水平。阿司匹林处理或幽门结扎后胃液中发现的高己糖胺总量,通过注射Fr.I-L或西咪替丁而降低。组织化学观察显示,Fr.I-L与保泰松或阿司匹林联合给药可防止胃上皮细胞中苏木精-伊红、过碘酸希夫和阿尔辛蓝染色多糖的消失。

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