格杜宁通过抑制NF-κB通路来缓解菌引起的皮肤炎症
Ju Kyoung Sim1, Ye Ji Heo1, Jin Hak Shin1
1Department of Molecular Bioscience, College of Biomedical Science, Kangwon National University, Chuncheon 24341, Republic of Korea.
Pharmaceuticals (Basel, Switzerland)
|January 25, 2025
概括
来自尼姆的基杜宁通过向NF-κB通路,有效降低了由Cutibacterium acnes (C. acnes) 引起的炎症. 这项研究表明,Gedunin.
科学领域:
- 皮肤病学和免疫学
- 自然产品化学 自然产品化学
- 分子生物学分子生物学
背景情况:
- 昆虫细菌 (C. acnes) 的细菌感染会触发炎症性细胞因子的产生,导致.
- 吉杜宁是阿扎迪拉赫塔印加 (neem) 的一种类植物,具有已知的抗炎性质.
- 吉杜宁在C. acnes引起的皮肤炎症中的抗炎作用目前尚未被探索.
研究的目的:
- 为了研究基杜宁对C. acnes引起的皮肤炎症的抗炎作用.
- 阐明基杜宁作用的基础分子机制.
- 评估格杜宁在治疗中的治疗潜力.
主要方法:
- 在RAW 264.7巨细胞和骨髓衍生巨细胞 (BMDMs) 中评估了基杜宁的抗炎活性.
- 测量的主要炎症调解剂:IL-1β,TNF-α,iNOS,COX-2和IL-6.
- 研究了NF-κB,MAPK信号通路和NLRP3炎症酶激活的参与.
- 利用体内小鼠模型来评估治疗疗效.
主要成果:
- 格杜宁显著降低了巨细胞中IL-1β,TNF-α,iNOS,COX-2和IL-6的表达.
- 葛杜宁抑制了NF-κB激活,但没有影响MAPK通路 (JNK/SAPK,ERK,p38 MAPK).
- 在BMDM中,葛杜宁抑制了NLRP3炎症酶激活.
- 在体内,格杜宁通过准NF-κB信号传递,有效地缓解了C. acnes诱导的炎症.
结论:
- 葛杜宁对C. acnes引起的皮肤炎症表现出显著的抗炎作用.
- 葛杜宁的治疗潜力通过抑制NF-κB信号传递来实现.
- 格杜宁代表了一种有前途的天然化合物,用于开发新的治疗方法.
相关概念视频
NF-κB-dependent Signaling Pathway
7.2K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
7.2K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
114
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...
114
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
141
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...
141
Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids
95
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...
95
TGF - β Signaling Pathway
7.2K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.2K
Drugs for Treatment of Ulcerative Colitis in IBD
118
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...
118


