过氧化剂通过改善TFEB介导的线粒体功能障碍来减轻罗二类类素诱导的肝损伤
Jie Xu1,2,3, Aizhen Xiong1,3, Xunjiang Wang1,3
1Shanghai Key Laboratory of Complex Prescriptions, The MOE Key Laboratory for Standardization of Chinese Medicines and the SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Traditional Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Cai Lun Road 1200, Zhangjiang, Shanghai, 201203, China.
Archives of pharmacal research
|September 21, 2023
概括
超氧化物 (Hyp) 通过激活TFEB通路,增强自和线粒体功能,保护皮罗利兹类 (PA) 诱导的肝损伤. 这表明Hyp Hyp.
科学领域:
- 肝病学和毒理学研究
- 分子生物学和细胞通路.
- 自然产品药物发现自然产品药物发现
背景情况:
- 罗胺类化合物 (PAs) 是已知的肝毒素,可引起严重的肝损伤.
- 超氧化物 (Hyp) 是一种天然的黄类化合物,具有肝保护性,但其对抗PA引起的损伤的机制尚不清楚.
- 了解Hyp的作用对于开发新型治疗PA诱导的肝毒性至关重要.
研究的目的:
- 为了研究超氧化物 (Hyp) 对化 (PA) 诱导的肝损伤的保护作用.
- 阐明潜在的分子机制,重点关注TFEB-PGC1α通路,自和线粒体生物发生.
- 评估mTORC1信号传导在调解Hyp的保护作用中的作用.
主要方法:
- 建立体外 (小鼠初级肝细胞) 和体内 (小鼠模型) 系统,用于PA诱导的肝损伤.
- RNA测序以确定受Hyp治疗影响的关键分子通路.
- 对mTORC1信号的药理学操纵,以确认其在保护机制中的作用.
主要成果:
- 过氧化物 (Hyp) 在体外和体外模型中显著减弱了PA诱导的肝毒性.
- RNA测序显示,Hyp的益处与转录因子EB (TFEB) -PGC1α通路有关.
- 催眠促进了TFEB核转移,激活了自 - lysosomal通路和线粒体生物发生,同时抑制了mTORC1活动增强了这些效应.
结论:
- 超氧化物 (Hyp) 通过通过mTORC1抑制激活TFEB介导的自和线粒体生物发生,从而防止PA诱导的肝损伤.
- 这项研究强调了Hyperoside在治疗PA诱导的肝毒性方面的治疗潜力.
- 这些发现为使用Hyp作为PAs.肝损伤的保护剂提供了机制基础.
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