相关实验视频
Updated: Jan 10, 2026

07:48
Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia
Published on: June 8, 2019
9.2K
IL17A 中介糖溶解依赖的初级血管生成,并加剧缺血性中风损伤
Qingxue Xu1,2, Zhengqi Lian1,2, Yingze Ye1,2
1Central Laboratory, Renmin Hospital of Wuhan University, 99 Zhangzhidong Road, Wuhan, 430060, Hubei Province, China.
Molecular neurobiology
|November 25, 2025
概括
干白素-17A (IL17A) 通过促进缺陷的血脑屏障修复和增加炎症来恶化缺血性中风. 这导致大脑损伤和中风后恢复受损.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 血管生物学 血管生物学
背景情况:
- 缺血性中风导致高死亡率和残疾,原因是治疗窗口有限,以及破坏血脑屏障 (BBB) 的炎症反应.
- 干白素-17A (IL17A) 是一种炎症因子,与中风后炎症有关,但它在BBB中断和脑损伤中的精确作用需要进一步调查.
- 了解IL17A的机制对于开发有针对性的疗法以减轻缺血性中风损伤至关重要.
研究的目的:
- 调查IL17A如何调节血管生成,加剧BBB透性,并导致缺血性中风中脑损伤.
- 在缺血性中风的背景下阐明IL17A的有害机制.
- 探索IL17A诱导血管生成的作用及其对糖解的依赖.
主要方法:
- 通过IL17A注射建立了一个中脑动脉封闭 (MCAO) 鼠标模型.
- 评估神经行为功能 (Longa评分),心脏病发作量 (TTC染色) 和蛋白质表达 (西方斑).
- 在体外和体内评估的BBB透性 (埃文斯蓝色,IgG染色),紧密结 (TEM) 和亡 (TUNEL).
主要成果:
- 在MCAO小鼠中,IL17A促进了缺陷血管生成,增加了炎症细胞透,并加剧了脑梗塞.
- 缺陷的血管生成导致了矩阵金属蛋白酶的分泌,紧密结的降解,并增加了BBB的透性.
- 由IL17A诱导的血管生成依赖于糖解来获得能量,有利于细胞存活而不是细胞亡.
结论:
- 在急性缺血性中风期间,IL17A促进了"缺陷血管生成",增加了BBB的透性和炎症透.
- IL17A可以提高MMP-9的调节,降低紧张的结节和恶化缺血性脑损伤.
- 针对IL17A介导途径,特别是糖解,可能为缺血性中风提供治疗潜力.
相关概念视频
Regulation of Angiogenesis and Blood Supply
3.3K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.3K
Mechanism of Angiogenesis
6.6K
Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
6.6K
Inflammatory Response I: Vascular and Cellular
15.9K
The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
15.9K
PI3K/mTOR/AKT Signaling Pathway
5.3K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
5.3K
TGF - β Signaling Pathway
10.4K
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...
10.4K

