凯姆菲罗尔通过NF-κB通路保护肠血管屏障免受高葡萄糖诱导的疾病
Tianjiao Chu1, Ruyang Yu2, Yinping Gu2
1Innovation Research Institute of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Ji'nan, PR China.
The Journal of nutritional biochemistry
|October 23, 2023
概括
凯姆菲罗尔通过保持紧密的结节和减少炎症来保护肠血管屏障免受高葡萄糖损伤. 这种天然化合物抑制了与高血糖相关的胃肠道问题相关的关键途径.
科学领域:
- 生物化学 生化学
- 分子生物学分子生物学
- 胃肠病学 胃肠病学
背景情况:
- 高血糖水平可能会损害肠血管屏障 (GVB),导致胃肠道疾病.
- 凯姆菲罗尔对肠道炎症的保护作用背后的分子机制尚未完全理解.
研究的目的:
- 在高葡萄糖条件下研究卡姆菲罗尔对GVB的保护作用.
- 阐明凯姆菲罗尔施加其保护作用的分子机制.
主要方法:
- 用大鼠肠道微血管内皮细胞 (RIMVECs) 来评估屏障透性.
- 埃文斯蓝色白蛋白流量试验被用来测量内皮细胞的透性.
- 西方涂抹和免疫光被用于分析蛋白质表达和局部化 (Claudin-5,VEGFR2,p38,ICAM-1,VCAM-1,NF-κB p65).
主要成果:
- 在RIMVEC中,kaempferol (50μM) 逆转了高葡萄糖诱导的屏障透性和Claudin-5稀释.
- 凯姆菲罗尔通过抑制VEGFR2/p38通路来抑制高葡萄糖诱导的血管生成和细胞迁移.
- 凯姆菲罗尔通过抑制NF-κB p65核转位来减少ICAM-1和VCAM-1的过度产生,类似于NF-κB抑制剂SN50.
结论:
- 凯姆菲罗尔可以保护肠血管屏障免受高葡萄糖引起的损伤.
- 凯姆菲罗尔通过调节VEGFR2/p38和NF-κB通路来发挥其保护作用.
- 这些发现为缓解高血糖症相关的胃肠道炎症的kaempferol机制提供了新的视角.
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