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在糖尿病血管并发症中通过ROS和p38MAPK/JNK途径诱导EPC的AGE

X Yang¹, Z Zhu, Z Li

¹Department of General Surgery (Vascular Surgery), the Affiliated Hospital of Southwest Medical University, Luzhou, China. huhubaby216@163.com.

Physiological research

|August 31, 2025

概括

通过氧化应激和MAPK通路,高级糖化终产物 (AGEs) 诱导内皮前体细胞 (EPC) 的亡,从而导致糖尿病的血管损伤. 抗氧化剂和MAPK抑制剂可以减轻由AGE引起的EPC亡.

科学领域:

细胞生物学
血管生物学
糖尿病学

背景情况:

内皮前体细胞 (EPC) 对于血管修复至关重要.
糖尿病加快血管损伤,部分原因是EPC亡的增加.
先进的糖化终产物 (AGE) 与糖尿病并发症有关,但它们对EPC的直接影响尚不清楚.

研究的目的:

通过氧化应激和MAPK激活来调查AGE是否会诱导EPC亡.
阐明AGE诱导的EPC亡的潜在分子机制.

主要方法:

从大鼠骨髓中分离出EPC,并用不同的AGE度和持续时间进行治疗.
使用Annexin V/ PI染色和流细胞测量进行了亡的评估.
分析了Bax和Bcl-2蛋白质水平,以及活性氧物种 (ROS) 生成和MAPK通路激活 (JNK,p38MAPK).
评估了N-乙半氨酸 (NAC),SP600125和SB203580的作用.

主要成果:

随着剂量和时间的变化,AGE显著增加了EPC亡.
治疗AGE增加了Bax表达,降低了Bcl-2表达,并增加了ROS生成.
抗氧化剂NAC和MAPK抑制剂 (SP600125,SB203580) 减弱了AGE诱导的亡,ROS产生,并调节了Bax/ Bcl-2水平.

结论:

通过氧化应激和JNK和p38MAPK通路的激活,AGEs会触发EPC亡.
通过保护EPC,针对氧化应激和MAPK信号可能为糖尿病血管并发症提供治疗策略.

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