桑托胡摩尔通过通过AMPK/Akt/GSK3β通路的Nrf2激活来保护对乙氨基诱导的肝毒性
Laiyu Zhu1, Xiaoye Fan1, Chunyuan Cao2
1Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin 130001, China.
概括
香醇通过减少氧化应激和线粒体损伤来保护肝脏免受乙氨基过量. 它激活Nrf2通路,为乙胺诱导的肝毒性提供了潜在的治疗策略.
科学领域:
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
- 肝病学 肝病学是一种肝病学.
背景情况:
- 乙氨基 (APAP) 过量服用是导致急性肝衰竭的主要原因.
- 对抗APAP诱导的肝损伤的桑托胡摩尔的保护机制尚未完全理解.
研究的目的:
- 为了研究黄醇对APAP诱导的肝毒性的肝保护作用和潜在机制.
- 阐明AMPK/Akt/GSK3β/Nrf2通路在桑托摩尔的保护作用中的作用.
主要方法:
- 使用APAP诱导的HepG2细胞进行体外研究,以评估细胞毒性和氧化应激.
- 在体内研究使用APAP诱导的急性肝损伤的小鼠模型.
- 对与氧化应激,炎症和亡相关的关键分子标记物的分析.
主要成果:
- 香醇通过AMPK/Akt/GSK3β通路对Nrf2的表达进行上调,抑制了HepG2细胞中APAP诱导的细胞毒性和氧化应激.
- 在体内,香醇降低了APAP诱导的死亡率,肝酶升高,氧化应激和组织病理损伤.
- 桑托胡摩尔抑制了JNK,Bax,cytochrome c,AIF和Caspase-3的激活,同时促进了Nrf2的核转录和激活AMPK/Akt/GSK3β通路.
结论:
- 赞索醇显示出对APAP诱导的肝损伤有显著的肝保护作用.
- 保护机制涉及通过AMPK/Akt/GSK3β/Nrf2抗氧化途径抑制氧化应激和线粒体功能障碍.
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