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阿斯蒂尔宾通过p53-中介抑制氧化损伤和亡,在肺损伤中提供辐射保护
Qian-Xin Hu1,2,3, Xue Ou1,4, Ya-Qin Huang1,2
1Department of Radiation Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.
Chinese journal of integrative medicine
|March 13, 2026
概括
阿斯提尔 (AST) 通过抑制p53乙化 (Ap53),减少氧化应激,DNA损伤和亡来预防辐射诱导的肺损伤 (RILI). 这些保护作用在野生类型的p53细胞和小鼠中被观察到,但在突变的p53模型中没有.
科学领域:
- 分子生物学分子生物学
- 辐射瘤学 辐射瘤学
- 药理学 药理学是指药理学的学科.
背景情况:
- 辐射诱导的肺损伤 (RILI) 是一个重大的临床挑战.
- 在RILI病原体中p53乙化 (Ap53) 的作用需要进一步阐明.
- 阿斯蒂尔 (AST) 是一种具有潜在治疗功能的天然化合物.
研究的目的:
- 调查AST对RILI的保护作用背后的分子机制.
- 为了确定p53乙化在AST减轻RILI中的作用,在体外和体内.
主要方法:
- 在体外研究中,在野生型 (WT) 和突变型 (Mut) p53肺上皮细胞 (TC-1) 上使用了辐射和AST治疗.
- 试验包括西斑,免疫光,TUNEL和流细胞计,以测量Ap53,γ-H2AX,亡和ROS.
- 在体内研究中,WT和p53-Knockout (KO) 的小鼠接受了AST治疗,并接受了全胸部辐射,随后进行了组织学和IHC分析.
主要成果:
- 在WT-p53细胞中,AST显著降低了Ap53,ROS,γ-H2AX和亡,但在Mut-p53细胞中没有影响.
- 在体内,AST在p53-WT小鼠中减轻了RILI,但在p53-KO小鼠中没有.
- 在p53-WT小鼠的肺部中,AST降低了p53蛋白和Ap53水平,但在p53-KO小鼠中没有影响.
结论:
- 阿斯蒂尔宾减轻了辐射诱导的氧化应激,DNA损伤和亡.
- AST对RILI的保护机制包括抑制p53乙化 (Ap53).
- AST显示了预防和缓解RILI的治疗潜力,特别是在涉及功能p53.3的环境中.
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