达帕格利弗洛辛改善多克索鲁比辛诱导的脑化学反应和老鼠的认知异常: AKT/GSK-3β和Wnt/β-catenin通路的调节
Gehad Farouk Abdelhafez1, Sylvia A Boshra1, Hagar B Abo-Zalam2
1Biochemistry Department, Faculty of Pharmacy, October 6 University, Giza, Egypt.
Neurochemical research
|September 5, 2025
概括
在大鼠中,达帕格利弗洛辛 (DAPA) 能预防多克索鲁比辛 (DOX) 诱导的认知衰退. DAPA具有抗氧化,抗炎和抗丧作用,减轻神经退化和改善认知功能.
科学领域:
- 神经科学
- 药理学
- 癌症学
背景情况:
- 化疗,特别是多克索鲁比辛 (DOX),可能会导致癌症幸存者的认知障碍.
- 这些损伤与氧化应激,神经炎症和亡有关.
- 达帕格利弗洛辛 (DAPA) 具有有前途的抗氧化,抗炎和抗丧性质.
研究的目的:
- 调查达帕格利弗洛辛 (DAPA) 对多克索鲁比辛 (DOX) 诱导的神经退行和认知功能障碍的神经保护潜力.
- 阐明DAPA神经保护的基本机制.
主要方法:
- 在使用多克索鲁比辛 (DOX) 的老鼠中诱导化学蛋白.
- 鼠被用达帕格利弗洛辛 (DAPA) 治疗了28天.
- 进行了认知行为测试,组织病理分析和分子测试.
主要成果:
- DAPA显著改善了认知功能,并逆转了DOX诱导的组织病理变化.
- DAPA降低了氧化应激标志物 (NOX4,MDA) 和增加了抗氧化酶 (SOD,GSH).
- DAPA抑制了神经炎症 (IL-1β,TNF-α,NF-κB) 和亡 (Caspase-3,AKT/GSK-3β,Wnt/β-catenin通路) 的发生.
结论:
- 达帕格利弗洛辛 (DAPA) 提供神经保护,防止多克索鲁比 (DOX) 引起的认知缺陷.
- DAPA的治疗作用是由其抗氧化,抗炎和抗丧作用介导的.
- DAPA 是一种潜在的治疗策略来治疗化疗引起的认知障碍.
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