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Updated: Jul 27, 2025

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在西斯普拉丁诱导的神经管缩中p53的作用

Chinami Matsumoto¹, Hitomi Sekine¹, Nana Zhang¹

¹Tsumura Kampo Research Laboratories, Tsumura & Co., 3586 Yoshiwara, Ami-machi, Inashiki-gun 300-1192, Japan.

International journal of molecular sciences

|June 10, 2023

概括

西斯普拉丁化学疗法通过激活p53并增加肌肉退化,导致肌肉损失. 一种p53抑制剂降低了这种效果,表明p53抑制剂会减少这种效果.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
癌症研究癌症研究

背景情况:

化疗诱导的肉会对癌症患者的预后和生活质量产生负面影响.
西斯普拉丁通过线粒体功能障碍和激活肌肉特异性泛基因酶 (Atrogin-1, MuRF1) 引起骨肌肉损失.
目前尚不清楚p53在西斯普拉丁诱导的肌肉缩中的作用.

研究的目的:

调查p53抑制剂pifithrin-alpha (PFT-α) 对C2C12神经管中西斯普拉丁诱导的肌肉缩的影响.
为了阐明p53通路在西斯普拉丁诱导的骨肌肉消耗中的参与.

主要方法:

C2C12神经管用西斯普拉丁和/或PFT-α进行治疗.
评估的p53和化p53蛋白水平.
测量了p53目标基因的mRNA表达 (PUMA,p21,Bax,Bcl-2,MuRF1,Atrogin-1). 通过测量p53目标基因的mRNA表达 (PUMA,p21,Bax,Bcl-2,MuRF1,Atrogin-1).
评估了细胞内活性氧物种 (ROS) 生产和线粒体功能.
量化了髓酸重链,肌肉特异性动蛋白和肌球蛋白水平.

主要成果:

西斯普拉丁增加了p53激活和p53向基因表达 (PUMA,p21).
PFT-α治疗缓解了西斯普拉丁诱导的ROS产生,线粒体功能障碍和Bax/Bcl-2比率的增加.
通过PFT-α降低了cisplatin诱导的MuRF1和Atrogin-1基因表达的上调.
PFT-α并没有阻止肌重链,肌肉特异性动因或肌球蛋白水平的下降.

结论:

西斯普拉丁通过一种p53依赖的机制诱导C2C12神经管中的肌肉降解.
p53在西斯普拉丁诱导的肌肉蛋白分解中起作用.
在西斯普拉丁治疗期间,p53似乎在减少肌肉蛋白质合成方面发挥的作用很小.

关键词:

在C2C12神经管中.缩性缩 (英语:Atrophy atrophy) 是一种损伤.西斯普拉丁 (cisplatin) 是一种制剂.在 p53 里,p53 是一个 p53 的类型.皮菲思林-阿尔法是什么

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