富含的溶液通过调节氧化应激和巨细胞两极分化来缓解急性辐射肺炎
Zhen Yin1, Wenjing Xu1, Junjun Ling1
1Department of Oncology, Chongqing Traditional Chinese Medicine Hospital, 400021, Chongqing, China.
Journal of radiation research
|April 8, 2024
概括
富含的溶液 (HRS) 通过减少炎症和氧化应激减轻老鼠的急性辐射肺炎 (ARP). 此外,HRS治疗还可以激活自和调节AMPK/mTOR/ULK1通路,改善肺组织损伤.
科学领域:
- 肺部医学 肺部医学
- 放射学 放射学是一门学科.
- 细胞生物学 细胞生物学
背景情况:
- 急性辐射肺炎 (ARP) 是胸部放射治疗的一个显著副作用.
- 目前对ARP的治疗方法有限,需要探索新的治疗策略.
- 理解ARP背后的分子机制,包括炎症和氧化应激,对于开发有效的干预措施至关重要.
研究的目的:
- 在大鼠模型中研究富含溶液 (HRS) 对辐射诱导的急性辐射肺炎 (ARP) 的治疗作用.
- 阐明HRS作用的潜在机制,重点关注巨细胞两极分化,线粒体氧化应激和自.
- 为了检查腺5'-单酸盐激活蛋白激酶的作用/哺乳动物目标的拉帕米辛/Unc-51-like激酶1 (AMPK/mTOR/ULK1) 信号通路在HRS介导的防护ARP.
主要方法:
- 使用X射线照射建立ARP大鼠模型.
- 使用HE和马森染色剂评估组织病理学变化.
- 通过ELISA和流细胞计量来量化炎症性细胞因子和巨分极 (M2/M1比).
- 评估线粒体氧化应激指标使用西斑,RT-qPCR和流细胞计.
- 对自标记物和AMPK/mTOR/ULK1信号通路的分析,通过西部斑点和免疫光.
主要成果:
- ARP诱导了显著的肺损伤,增加了原沉积,巨细胞透和M1极化.
- 治疗HRS缓解了病理损伤,抑制了M1极化,并减少了炎症反应.
- HRS逆转了ARP诱导的线粒体氧化应激和自抑制.
- 治疗HRS调节了AMPK/mTOR/ULK1通路,抑制AMPK-α酸化,同时激活mTOR和ULK1酸化.
结论:
- 富含的溶液对急性辐射肺炎具有显著的治疗潜力.
- HRS通过抑制M1巨细胞极化,减轻氧化应激和激活自来发挥其保护作用.
- AMPK/mTOR/ULK1信号通路是HRS在ARP中的有益作用的关键调解者.
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