Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

244
Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide...
244
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

278
Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
278
T Cell Types and Functions01:24

T Cell Types and Functions

1.4K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.4K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

240
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
240
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

345
Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
345
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

210
Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
210

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Cascade Oxidation of Ethylene and Propylene over a Redox Heterometallic Cluster.

Journal of the American Chemical Society·2026
Same author

Aerobic exercise attenuates cardiac fibrosis in mice via stimulating vitamin D receptor to suppress ferroptosis.

Molecular and cellular endocrinology·2026
Same author

Reporting quality and evidence support in randomized controlled trials of Bupleurum-based herbal medicine formulas for epilepsy.

Journal of ethnopharmacology·2026
Same author

Vitamin D receptor/sirtuin 3 pathway mediates the cardioprotective effects of aerobic exercise in diabetic mice.

Free radical biology & medicine·2026
Same author

Particles, deposits and sediments: unravelling the complexities of IOL opacification.

International journal of ophthalmology·2026
Same author

Inhibition of d-ribose-induced glycation of metalloprotein human myoglobin by bioactive quinones.

Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy·2026

相关实验视频

Updated: Sep 18, 2025

Therapeutic Evaluation of Fecal Microbiota Transplantation in an Interleukin 10-Deficient Mouse Model
05:41

Therapeutic Evaluation of Fecal Microbiota Transplantation in an Interleukin 10-Deficient Mouse Model

Published on: April 6, 2022

3.0K

通过减少ISG15表达,IL-10通过调节线粒体功能来缓解性结肠炎.

Zhi He1, Ya-Dong Feng2, Yue-Xin Zhang1

  • 1Center of Clinical Laboratory Medicine, Zhongda Hospital, Southeast University, 87 Ding Jiaqiao, Nanjing 210009, China.

Cellular signalling
|June 20, 2025
PubMed
概括

介质素-10 (IL-10) 通过减少炎症和修复肠道屏障,有效治疗性结肠炎 (UC). 这种细胞因子治疗激活了自和调节ISG15表达,为UC患者提供了一个有前途的治疗策略.

关键词:
自自是一种自的过程.在 IL-10 中,IL-10 是 IL-10 的代表.在ISG15中,我们可以看到ISG15.肠道屏障 肠道屏障 肠道屏障线粒体功能 线粒体功能性结肠炎是一种

更多相关视频

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

16.8K
Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

2.7K

相关实验视频

Last Updated: Sep 18, 2025

Therapeutic Evaluation of Fecal Microbiota Transplantation in an Interleukin 10-Deficient Mouse Model
05:41

Therapeutic Evaluation of Fecal Microbiota Transplantation in an Interleukin 10-Deficient Mouse Model

Published on: April 6, 2022

3.0K
Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

16.8K
Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

2.7K

科学领域:

  • 胃肠病学 胃肠病学
  • 免疫学 免疫学 免疫学
  • 分子生物学分子生物学

背景情况:

  • 介素-10 (IL-10) 是一种抗炎性细胞因子,在自身免疫性疾病中具有潜在的治疗应用.
  • 对于IL-10对性结肠炎 (UC) 的特定影响尚不完全理解.
  • 这项研究调查了IL-10在抑制UC爆发中的有效性.

研究的目的:

  • 评估介质素-10 (IL-10) 在治疗性结肠炎 (UC) 中的治疗潜力.
  • 阐明IL-10对肠道炎症,亡和氧化应激的影响背后的分子机制.

主要方法:

  • 通过使用硫酸 (DSS) 建立了UC的小鼠模型.
  • 利用脂聚糖 (LPS) 刺激的Caco-2细胞来研究分子通路.
  • 分析了干扰素刺激基因15 (ISG15) 表达和自标志物 (ATG7,LC3-II/LC3-I比率).

主要成果:

  • 服用IL-10显著改善了DSS诱导的大肠炎的临床结果,包括体重恢复和结肠长度增加.
  • 通过抑制亡,减少促炎细胞因子,调节氧化应激标志物,IL-10保护了肠道上皮细胞.
  • IL-10增强了自,抑制了ISG15的上调,并减少了Caco-2细胞的亡和氧化应激;这些效应被自抑制或ISG15过度表达所废除.

结论:

  • 通过激活自和调节ISG15,IL-10的使用有效地抑制了UC的进展.
  • 针对性地将IL-10输送到肠膜本身,可以提高治疗效果,并最大限度地减少副作用.