• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

相似文献

1
Inflammatory bowel disease-like enteritis and caecitis in a senescence accelerated mouse P1/Yit strain.衰老加速小鼠P1/Yit品系中的炎症性肠病样肠炎和盲肠炎
Gut. 1998 Jul;43(1):71-8. doi: 10.1136/gut.43.1.71.
2
Preventive effects of Bifidobacterium- and Lactobacillus-fermented milk on the development of inflammatory bowel disease in senescence-accelerated mouse P1/Yit strain mice.双歧杆菌和乳酸杆菌发酵乳对衰老加速小鼠P1/Yit品系小鼠炎症性肠病发展的预防作用。
Digestion. 2001;64(2):92-9. doi: 10.1159/000048846.
3
Pathogenesis of gastritis in ileitis-prone SAMP1/Yit mice.易患回肠炎的SAMP1/Yit小鼠胃炎的发病机制。
Keio J Med. 2011;60(2):65-8. doi: 10.2302/kjm.60.65.
4
Blockade of PSGL-1 attenuates CD14+ monocytic cell recruitment in intestinal mucosa and ameliorates ileitis in SAMP1/Yit mice.阻断PSGL-1可减少肠道黏膜中CD14+单核细胞的募集，并改善SAMP1/Yit小鼠的回肠炎。
J Leukoc Biol. 2005 Mar;77(3):287-95. doi: 10.1189/jlb.0204104. Epub 2004 Nov 29.
5
In vivo demonstration of T lymphocyte migration and amelioration of ileitis in intestinal mucosa of SAMP1/Yit mice by the inhibition of MAdCAM-1.通过抑制黏膜地址素细胞黏附分子-1（MAdCAM-1）在SAMP1/Yit小鼠肠道黏膜中进行T淋巴细胞迁移的体内验证及回肠炎的改善
Clin Exp Immunol. 2005 Apr;140(1):22-31. doi: 10.1111/j.1365-2249.2005.02742.x.
6
Omega-3 polyunsaturated fatty acids ameliorate the severity of ileitis in the senescence accelerated mice (SAM)P1/Yit mice model.ω-3 多不饱和脂肪酸可改善快速老化小鼠（SAM）P1/Yit 模型中回肠炎的严重程度。
Clin Exp Immunol. 2009 Dec;158(3):325-33. doi: 10.1111/j.1365-2249.2009.04020.x. Epub 2009 Sep 30.
7
Decreased production of interleukin-10 and transforming growth factor-β in Toll-like receptor-activated intestinal B cells in SAMP1/Yit mice.SAMP1/Yit 小鼠肠道 Toll 样受体激活的 B 细胞中白细胞介素-10 和转化生长因子-β产生减少。
Immunology. 2010 Dec;131(4):473-87. doi: 10.1111/j.1365-2567.2010.03318.x.
8
STAT3 activation via interleukin 6 trans-signalling contributes to ileitis in SAMP1/Yit mice.通过白细胞介素6转信号传导激活STAT3会导致SAMP1/Yit小鼠患回肠炎。
Gut. 2006 Sep;55(9):1263-9. doi: 10.1136/gut.2005.079343. Epub 2006 May 8.
9
Emergence of perianal fistulizing disease in the SAMP1/YitFc mouse, a spontaneous model of chronic ileitis.SAMP1/YitFc小鼠（一种慢性回肠炎自发模型）中出现肛周瘘管病。
Gastroenterology. 2003 Apr;124(4):972-82. doi: 10.1053/gast.2003.50148.
10
Interleukin-5 participates in the pathogenesis of ileitis in SAMP1/Yit mice.白细胞介素-5参与SAMP1/Yit小鼠回肠炎的发病机制。
Eur J Immunol. 2004 Jun;34(6):1561-9. doi: 10.1002/eji.200324680.

引用本文的文献

1
Human placenta mesenchymal stromal cells alleviate intestinal inflammation and repair intestinal barrier function by activating AMPK-FXR pathway.人胎盘间充质基质细胞通过激活AMPK-FXR通路减轻肠道炎症并修复肠道屏障功能。
Commun Biol. 2025 May 30;8(1):830. doi: 10.1038/s42003-025-08261-y.
2
A Similar Mutation in the AAUU-Rich Elements of the Mouse TNF Gene Results in a Distinct Ileocolitic Phenotype: A New Strain of TNF-Overexpressing Mice.小鼠TNF基因富含AAUU元件中的类似突变导致独特的回结肠炎症表型：一种新的TNF过表达小鼠品系。
Inflamm Bowel Dis. 2025 Apr 10;31(4):1067-1081. doi: 10.1093/ibd/izae307.
3
Fibrosis in IBD: from pathogenesis to therapeutic targets.炎症性肠病中的纤维化：从发病机制到治疗靶点。
Gut. 2024 Apr 5;73(5):854-866. doi: 10.1136/gutjnl-2023-329963.
4
Current status and future prospects of stomatology research.口腔医学研究的现状与展望。
J Zhejiang Univ Sci B. 2023 Aug 7;24(10):853-867. doi: 10.1631/jzus.B2200702.
5
Animal models of inflammatory bowel disease: novel experiments for revealing pathogenesis of colitis, fibrosis, and colitis-associated colon cancer.炎症性肠病的动物模型：揭示结肠炎、纤维化和结肠炎相关结肠癌发病机制的新实验
Intest Res. 2023 Jul;21(3):295-305. doi: 10.5217/ir.2023.00029. Epub 2023 May 31.
6
Inhibition of Soluble Stem Cell Factor Promotes Intestinal Mucosal Repair.可溶性干细胞因子抑制促进肠道黏膜修复。
Inflamm Bowel Dis. 2023 Jul 5;29(7):1133-1144. doi: 10.1093/ibd/izad003.
7
Loss of autism-candidate CHD8 perturbs neural crest development and intestinal homeostatic balance.自闭症候选基因 CHD8 的缺失扰乱了神经嵴发育和肠道内稳态平衡。
Life Sci Alliance. 2022 Nov 14;6(1). doi: 10.26508/lsa.202201456. Print 2023 Jan.
8
Characterization of an intelectin-1 () knockout mouse model.鉴定凝集素-1（）基因敲除小鼠模型。
Front Immunol. 2022 Aug 22;13:894649. doi: 10.3389/fimmu.2022.894649. eCollection 2022.
9
Activity of isoflavone biochanin A in chronic experimental toxoplasmosis: impact on inflammation.染料木黄酮生物chanin A 在慢性实验性弓形虫病中的活性：对炎症的影响。
Parasitol Res. 2022 Aug;121(8):2405-2414. doi: 10.1007/s00436-022-07571-y. Epub 2022 Jun 17.
10
Contribution of the Gut Microbiota to Intestinal Fibrosis in Crohn's Disease.肠道微生物群对克罗恩病肠道纤维化的作用
Front Med (Lausanne). 2022 Feb 7;9:826240. doi: 10.3389/fmed.2022.826240. eCollection 2022.

本文引用的文献

1
Inflammatory bowel disease: an immunity-mediated condition triggered by bacterial infection with Helicobacter hepaticus.炎症性肠病：一种由肝螺杆菌细菌感染引发的免疫介导疾病。
Infect Immun. 1997 Aug;65(8):3126-31. doi: 10.1128/iai.65.8.3126-3131.1997.
2
Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses.白细胞介素-10缺陷小鼠的小肠结肠炎和结肠癌与细胞因子产生异常及CD4(+) TH1样反应有关。
J Clin Invest. 1996 Aug 15;98(4):1010-20. doi: 10.1172/JCI118861.
3
Expansion of alpha beta T-cell receptor-bearing intestinal intraepithelial lymphocytes after microbial colonization in germ-free mice and its independence from thymus.无菌小鼠微生物定植后，携带αβ T细胞受体的肠道上皮内淋巴细胞的扩增及其与胸腺的独立性。
Immunology. 1993 May;79(1):32-7.
4
Interleukin-10-deficient mice develop chronic enterocolitis.白细胞介素-10缺陷型小鼠会患上慢性小肠结肠炎。
Cell. 1993 Oct 22;75(2):263-74. doi: 10.1016/0092-8674(93)80068-p.
5
Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene.白细胞介素-2基因缺失小鼠中的溃疡性结肠炎样疾病
Cell. 1993 Oct 22;75(2):253-61. doi: 10.1016/0092-8674(93)80067-o.
6
Effects of fecal microorganisms and their chloroform-resistant variants derived from mice, rats, and humans on immunological and physiological characteristics of the intestines of ex-germfree mice.源自小鼠、大鼠和人类的粪便微生物及其耐氯仿变体对无菌小鼠肠道免疫和生理特性的影响。
Infect Immun. 1994 Dec;62(12):5442-6. doi: 10.1128/iai.62.12.5442-5446.1994.
7
Spontaneous, heritable colitis in a new substrain of C3H/HeJ mice.C3H/HeJ小鼠新亚系中的自发性遗传性结肠炎。
Gastroenterology. 1994 Dec;107(6):1726-35. doi: 10.1016/0016-5085(94)90813-3.
8
Regulatory interactions between CD45RBhigh and CD45RBlow CD4+ T cells are important for the balance between protective and pathogenic cell-mediated immunity.CD45RB高表达和CD45RB低表达的CD4⁺ T细胞之间的调节性相互作用对于保护性和致病性细胞介导的免疫之间的平衡很重要。
J Exp Med. 1994 Feb 1;179(2):589-600. doi: 10.1084/jem.179.2.589.
9
Phenotypically distinct subsets of CD4+ T cells induce or protect from chronic intestinal inflammation in C. B-17 scid mice.在C.B-17 scid小鼠中，表型不同的CD4+ T细胞亚群可诱导慢性肠道炎症或对其起到保护作用。
Int Immunol. 1993 Nov;5(11):1461-71. doi: 10.1093/intimm/5.11.1461.
10
Spontaneous intestinal inflammation and nitric oxide metabolism in HLA-B27 transgenic rats.HLA - B27转基因大鼠的自发性肠道炎症与一氧化氮代谢
Gastroenterology. 1995 Jul;109(1):142-50. doi: 10.1016/0016-5085(95)90279-1.

衰老加速小鼠P1/Yit品系中的炎症性肠病样肠炎和盲肠炎

Inflammatory bowel disease-like enteritis and caecitis in a senescence accelerated mouse P1/Yit strain.

作者信息

Matsumoto S, Okabe Y, Setoyama H, Takayama K, Ohtsuka J, Funahashi H, Imaoka A, Okada Y, Umesaki Y

机构信息

Yakult Central Institute for Microbiological Research, Tokyo, Japan.

出版信息

Gut. 1998 Jul;43(1):71-8. doi: 10.1136/gut.43.1.71.

DOI:10.1136/gut.43.1.71
PMID:9771408
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1727165/
Abstract

BACKGROUND

A new subline of the senescence accelerated mouse (SAM) P1/Yit strain has been established which shows spontaneous enteric inflammation under specific pathogen free (SPF) conditions.

AIMS

To elucidate the pathogenesis of enteric inflammation in this new subline.

METHODS

The SPF and germ free (GF) SAMP1/Yit strains were used. Histological, immunological, and microbiological characterisation of the mice with enteric inflammation was performed.

RESULTS

Histologically, enteritic inflammation developed as a discontinuous lesion in the terminal ileum and caecum with the infiltration of many inflammatory cells after 10 weeks of age. the activity of myeloperoxidase, and both immunolocalisation and mRNA expression of inducible nitric oxide synthase increased in the lesion. CD3-epsilon positive T cells, neutrophils, and macrophages were more numerous in the inflamed mucosa of the SAMP1/Yit strain. The GF SAMP1/Yit strain did not show any inflammation in the intestinal wall, by the age of 30 weeks, and the enteritis and caecitis developed 10 weeks after the conventionalisation of the GF SAMP1/Yit strain.

CONCLUSION

Enteric inflammation in the ileum and caecum developed in the SAMP1/Yit strain. The pathophysiological characteristics of the disease in this mouse have some similarities to those of human inflammatory bowel disease (IBD). This mouse strain should be a useful model system for elucidating the interaction between the pathogenesis of IBD and the gut microflora.

摘要

背景

已建立了衰老加速小鼠（SAM）P1/Yit品系的一个新亚系，该亚系在无特定病原体（SPF）条件下表现出自发性肠道炎症。

目的

阐明这个新亚系中肠道炎症的发病机制。

方法

使用SPF和无菌（GF）的SAMP1/Yit品系。对患有肠道炎症的小鼠进行组织学、免疫学和微生物学特征分析。

结果

组织学上，10周龄后，小肠末端和盲肠出现不连续病变，伴有大量炎性细胞浸润，形成肠炎。病变部位髓过氧化物酶活性、诱导型一氧化氮合酶的免疫定位及mRNA表达均增加。在SAMP1/Yit品系的炎症黏膜中，CD3-ε阳性T细胞、中性粒细胞和巨噬细胞数量更多。30周龄时，GF SAMP1/Yit品系的肠壁未出现任何炎症，在GF SAMP1/Yit品系常规饲养10周后发生肠炎和盲肠炎。

结论

SAMP1/Yit品系出现回肠和盲肠的肠道炎症。该小鼠疾病的病理生理特征与人类炎症性肠病（IBD）有一些相似之处。该小鼠品系应是阐明IBD发病机制与肠道微生物群之间相互作用的有用模型系统。