基于网络药理学探索柏柏林用于治疗糖尿病病的分子机制
Lin Yang1, Siming Yuan2, Rongrong Wang1
1Institute of Clinical Pharmacology, Key Laboratory of Anti-Infammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-Infammatory and Immune Medicine, Shushan District, Anhui Medical University, Hefei, Anhui 230032, China; Department of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.
柏柏林 (BBR) 通过向VEGFR2并影响PI3K/AKT/mTOR通路,显示出治疗糖尿病病 (DN) 的潜力. 这种机制抑制了中细胞的增殖,改善了糖尿病小鼠的功能.
科学领域:
- 药理学 药理学是指药理学的学科.
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
背景情况:
- 糖尿病病 (DN) 是一种常见的糖尿病并发症.
- 柏柏林 (BBR) 可能减轻DN,但其机制尚不清楚.
研究的目的:
- 研究BBR在治疗DN的分子机制.
- 确定BBR影响的关键目标和途径.
主要方法:
- 网络药理学用于识别BBR和DN目标.
- 生物信息学分析 (GO,KEGG,PPI) 的研究.
- 分子对接,CETSA,免疫光学和西欧斑点用于验证.
主要成果:
- 确定了92个重叠的目标;VEGFR2是BBR的一个关键目标.
- BBR与VEGFR2结合,从而抑制PI3K/AKT/mTOR通路的发生.
- 在体内,BBR降低了间细胞的增殖,改善了功能.
结论:
- BBR针对VEGFR2,调节PI3K/AKT/mTOR通路. 这一过程中,BBR对VEGFR2进行了定位.
- 这导致阻碍中细胞增殖和改善功能.
- BBR证明了糖尿病病的治疗潜力.
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