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斯基桑德林A通过EGFR/AKT/GSK3β信号通路减轻糖尿病病,基于网络药理学和实验验证

Pengyu Wang¹, Qing Lan¹, Qi Huang¹

¹School of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.

|August 28, 2024

概括

斯基桑德林A (Sch A) 通过改善葡萄糖耐受性和减少损伤,在老鼠中显示出对糖尿病病 (DN) 的保护作用. 它针对EGFR并调节AKT/GSK-3β通路,为DN提供了潜在的治疗策略.

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) 是末期病 (ESRD) 的主要原因之一.
斯基桑德林A (Sch A) 具有抗纤维素,抗质和抗氧化特性,但其在DN中的机制尚未完全理解.

研究的目的:

在糖尿病脏病 (DN) 的大鼠模型中研究斯基桑德林A (Sch A) 的治疗机制.
识别DN中SchA治疗影响的潜在治疗点和途径.

主要方法:

在老鼠中诱导的糖尿病病使用了链毒素 (STZ) 和高脂肪饮食,其次是施加SchA.
蛋白质与蛋白质相互作用 (PPI) 网络分析,基因和基因组的京都百科全书 (KEGG) 和基因本体学 (GO) 分析.
分子对接,H&E染色,Sirius红色染色,免疫组织化学,免疫光和西部斑点分析.

主要成果:

斯基桑德林A (Sch A) 改善了葡萄糖耐受性,减少了尿中的微蛋白和肌素,并减轻了DN大鼠的病理损伤.
皮肤表皮生长因子受体 (EGFR) 被确定为一个枢纽基因.
Sch A抑制了EGFR和PTRF蛋白表达,减少了与亡相关的蛋白质,并调节了AKT/GSK-3β信号通路.

结论:

斯基桑德林A (Sch A) 在糖尿病病 (DN) 鼠标模型中显示出显著的保护作用.
皮表皮生长因子受体 (EGFR) 是DN的潜在治疗点.
施加的治疗作用包括调节AKT/GSK-3β信号通路.

关键词:

在AKT/GSK-3ββ中.欧洲农业基金会 (EGFR) 是一个基金.斯基桑德林是一个A.糖尿病性脏病糖尿病脏病网络药理学网络药理学鼠标鼠标鼠标鼠标鼠标

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