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生物信息学和实验验证MAPK通路激活在由葡萄糖变性诱导的糖尿病病中的实验验证

Sujuan Li¹, Huijuan Wang², Yuanhang Zhang³

¹Department of Clinical Laboratory, Hangzhou Traditional Chinese Medicine Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China; Department of Pathology, 82nd Hospital of PLA, Huaian, Jiangsu, China.

Journal, genetic engineering & biotechnology

|December 12, 2025

概括

波动性高血糖导致糖尿病病 (DKD),通过氧化应激调节MAPK-JNK信号传递,涉及关键蛋白ITGB2和TYROBP. 这项研究阐明了DKD病变的分子机制.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
生物化学生物化学

背景情况:

糖尿病病 (DKD) 是糖尿病的一个主要并发症.
氧化应激在DKD的发病过程中起着至关重要的作用.
了解DKD的分子机制对于开发有效的治疗方法至关重要.

研究的目的:

评估与氧化应激诱导相关的因素在波动性高血糖诱导的DKD中的作用.
阐明了DKD病变的潜在分子机制.
确定参与DKD进展的关键蛋白质和信号通路.

主要方法:

从GEO数据库下载了基因表达数据集 (GSE30528,GSE30529).
使用STRING和Cytoscape识别了差异表达基因 (DEG) 和分析了蛋白质与蛋白质相互作用 (PPI) 网络.
进行了糖尿病动物实验,以验证已识别的蛋白质 (ITGB2,TYROBP) 和氧化应激在DKD中的作用.

主要成果:

确定ITGB2和TYROBP是参与MAPK级联调节的关键蛋白质.
糖尿病大鼠表现出改变的氧化应激标志物 (SOD,GSH-Px,MDA) 和JNK激活.
波动性高血糖被证明可以诱导亡反应,并通过氧化应激调节MAPK途径.

结论:

波动性高血糖直接和间接地通过ITGB2,TYROBP和氧化应激调节MAPK-JNK信号传递.
这些分子事件有助于糖尿病病的发病和进展.
这项研究提供了对DKD复杂病原学的见解.

关键词:

糖尿病病 (DKD) 是一种糖尿病性病.波动性葡萄糖的波动性是什么甲基因激活蛋白激酶 (MAPK) 是一种中基因激活蛋白激酶.氧化应激是一种氧化应激.

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