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通过给予同种异体抗原来诱导ICR小鼠发生萎缩性胃炎。

Induction of atrophic gastritis in ICR mice by the administration of an allogenic antigen.

作者信息

Watanabe H, Hirose F, Takizawa S, Terada Y

出版信息

Acta Pathol Jpn. 1977 Nov;27(6):799-808. doi: 10.1111/j.1440-1827.1977.tb03036.x.

DOI:10.1111/j.1440-1827.1977.tb03036.x
PMID:605795
Abstract

In an attempt to produce experimental autoimmunity in small animals the experiment was sought to induce atrophic gastritis in ICR/JCL mice. The stomach antigen of ICR mice was extracted and emulsified with an equal volume of Freund's complete adjuvant. This was subcutaneously injected in 5-week-old ICR/JCL mice at 1 week intervals for a total of 1 to 4 administrations. The stomach antibody in the serum gradually increased up to 2(6) until four weeks after the last injection of the stomach antigen. At the same time pyknosis and a decrease in number of the gastric mucosal cells, which ultimately led to the atrophying of gastric mucosa, developed. Thereafter, concomitant with the decrease in serum antibody against mucous cells, regeneration of mucous cells was especially remarkable, but atrophy of the fundic gland continued.

摘要

为了在小动物中诱导实验性自身免疫,尝试在ICR/JCL小鼠中诱发萎缩性胃炎。提取ICR小鼠的胃抗原,并与等体积的弗氏完全佐剂乳化。将其以1周的间隔皮下注射到5周龄的ICR/JCL小鼠中,总共注射1至4次。在最后一次注射胃抗原后的四周内,血清中的胃抗体逐渐增加至2(6)。与此同时,胃黏膜细胞出现核固缩且数量减少,最终导致胃黏膜萎缩。此后,随着针对黏液细胞的血清抗体减少,黏液细胞的再生尤为显著,但胃底腺的萎缩仍在继续。

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