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诺托金森化物R1可以抑制FGF1和VEGFA之间的相互作用,以减缓Podocyte亡

ChangYan Li¹, HuaChen Zhong², JingYuan Ma¹

¹Department of Nephrology, the First Affiliated Hospital of Kunming Medical University, No.295, Xichang Road, Kunming, Yunnan Province, 650032, China.

BMC endocrine disorders

|July 6, 2023

概括

诺托金化物R1 (NGR1) 抑制了血管内皮生长因子A (VEGFA) 和纤维细胞生长因子1 (FGF1) 之间的相互作用. 这种作用减缓了糖尿病脏病患者的 podocyte 亡,提供了一个潜在的治疗策略.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

糖尿病病 (DN) 涉及高葡萄糖环境中的微血管病,血管损伤通常与VEGFA相关.
传统的抗炎药物Notoginsenoside R1 (NGR1) 显示出血管活性.
鉴定在DN中保护血管炎症的药物至关重要.

研究的目的:

调查NGR1对糖尿病病中血管损伤的保护作用.
阐明NGR1作用背后的分子机制,重点关注VEGFA和FGF1相互作用.

主要方法:

使用Limma方法进行淋巴细胞转录组分析.
针对NGR1药物点的瑞士目标预测 (斯皮尔曼算法).
分子对接和共免疫沉 (COIP) 验证蛋白质相互作用.

主要成果:

NGR1通过键可能与VEGFA和FGF1结合.
NGR1 阻碍了 VEGFA 和 FGF1.1 之间的相互作用.
在高葡萄糖条件下,NGR1抑制了VEGFA和FGF1的表达,减缓了podocyte的亡.

结论:

NGR1 抑制了 FGF1-VEGFA 相互作用,从而减缓了 DN 中的 podocyte 亡.
通过减轻血管炎症和细胞死亡,NGR1显示出作为糖尿病病治疗剂的潜力.

关键词:

糖尿病脏病糖尿病脏病一个FGF1的FGF1.分子对接是分子对接.诺托基因化物R1 是一种诺托基因化物在VEGFA中,VEGFA是VEGFA.

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