整合网络药理学,以调查肉甲对抗氧化诱导的神经毒性的保护作用
Zhenzhu Zhai1, Mingzhu Li2, Huini Yao3
1Department of Integrated Traditional Chinese and Western Medicine Medical Oncology, Cancer Hospital of China Medical University, Cancer Hospital of Dalian University of Technology, Liaoning Cancer Hospital & Institute.
Journal of visualized experiments : JoVE
|December 15, 2025
概括
丁甲 (CA) 通过抑制JAK2/STAT3通路和激活SLC7A11-GSH-GPX4轴,减少氧化应激和铁死,保护大鼠背根结节细胞 (DRG) 免受氧化 (OXA) 诱导的损伤.
科学领域:
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 奥克沙利 (OXA) 化疗可以诱导神经毒性,特别是损害背部根结节 (DRG) 细胞.
- 已知药理作用的化合物甲 (CA) 正在研究其对这种损伤的保护潜力.
研究的目的:
- 为了研究 cinnamaldehyde (CA) 对大鼠背根 (DRG) 细胞的氧化 (OXA) 诱导的损伤的保护作用.
- 阐明潜在的分子机制,包括信号通路和关键蛋白质表达,参与CA的保护作用.
主要方法:
- 使用TCMSP,TCMIP和PharmMapper进行网络药理学分析,以确定潜在的目标.
- 细胞活力通过CCK-8试验评估;脂质过氧化量通过马隆迪甲 (MDA) 试验测量.
- 细胞内铁 (Fe2+) 和活性氧物种 (ROS) 用光探针量化.
- 通过免疫阻塞分析的蛋白质表达水平 (p-STAT3,XCT,GPX4).
主要成果:
- 网络药理学确定了14个与CA,神经病痛和铁死相关的重叠目标.
- 最佳CA度 (24小时内4.0μmol/L) 显著降低了DRG细胞中的MDA,Fe2+和ROS水平 (P <0.05).
- CA降低了JAK2,STAT3,p-STAT3,TFRC,ErbB-1和NF-κB的表达,同时上调了XCT,GPX4和FTH1的表达 (P <0.05).
结论:
- 丁甲 (CA) 有效地减轻了大鼠DRG细胞中氧化 (OXA) 诱导的损伤.
- CA通过抑制JAK2/STAT3信号通路来发挥其保护作用.
- 此外,CA还激活SLC7A11-GSH-GPX4轴,这表明它在预防铁亡和氧化应激方面发挥了作用.
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