卡诺索尔通过p62-KEAP1-NRF2信号通路减轻Ang II诱导的损伤
Shijie Fan1, Ying Zhao1, Qingqing Zhao1
1Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Toxicology and applied pharmacology
|August 23, 2025
概括
通过减少损伤和氧化应激,Carnosol有效治疗高血压病 (HRD). 它通过激活p62-KEAP1-NRF2通路而起作用,为相关损伤提供了潜在的新疗法.
科学领域:
- 肝脏病学
- 氧化应激研究
- 药理学
背景情况:
- 高血压是病的主要原因,特别是高血压病 (HRD).
- 在高血压相关的脏疾病中,还原平衡至关重要.
- 卡诺索尔 (Car) 是一种已知的抗氧化剂,但其在HRD中的作用尚未研究.
研究的目的:
- 研究Carnosol对高血压脏疾病的治疗作用.
- 阐明卡诺索尔在HRD中的作用的药理机制.
主要方法:
- 使用血管素II (Ang II) 诱导损伤和氧化应激的体外和体内实验.
- 用Carnosol (40 mg/kg) 来评估其作用.
- 分析p62-KEAP1-NRF2通路,包括mTOR和mTORC1信号.
主要成果:
- 卡诺索尔显著改善了Ang II诱导的损伤和氧化应激.
- 通过mTOR相互作用促进了p62酸化,导致KEAP1降解和NRF2激活.
- NRF2的上调导致抗氧化基因表达的增加.
- 抑制mTORC1消除了Carnosol对p62和抗氧化功能的作用.
结论:
- 卡诺索尔激活p62-KEAP1-NRF2通路以减轻Ang II诱导的HRD中的损伤和氧化应激.
- 卡诺索尔具有预防和治疗Ang II诱导的损伤的潜力.
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