棕酸通过抑制BMAL1-NAD+-SIRT2轴引起肝细胞炎症
Savera Aggarwal1, Archana Rastogi2, Rakhi Maiwall3
1Department of Molecular and Cellular Medicine, Institute of Liver and Biliary Sciences, Delhi, India.
Journal of physiology and biochemistry
|September 17, 2024
概括
棕酸通过破坏BMAL1-NAD+-SIRT2通路来诱导肝损伤. 激活这个轴可以保护肝细胞免受脂质诱导的炎症和毒性,为肝脏疾病提供潜在的治疗策略.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 分子生物学分子生物学
- 时间生物学 时间生物学
背景情况:
- 棕酸是一种常见的和脂肪酸,导致肝细胞毒性和炎症.
- 和脂肪酸可以破坏身体的自然昼夜节律.
- 时钟基因和NAD+依赖的Sirtuins在肝脏保护中的相互作用尚未完全理解.
研究的目的:
- 为了研究昼夜钟基因和Sirtuins在保护肝细胞免受棕酸诱导的损伤之间的联系.
- 探索BMAL1-NAD+-SIRT2轴在调节肝细胞中脂毒性和炎症中的作用.
主要方法:
- 肝细胞 (PH5CH8 和 HepG2) 用棕酸进行治疗.
- 评估了SIRT2和BMAL1的水平和活性.
- 测量了NAD+水平,炎症标志物和细胞活力.
- 分析了来自NASH患者的临床肝脏样本.
主要成果:
- 棕酸诱导脂肪酸,炎症,并降低了肝细胞中的NAD+水平.
- 棕酸降低了SIRT2蛋白水平,活性和BMAL1昼夜表达,特别是在非癌细胞中.
- 在肝硬化样本中,SIRT2和BMAL1水平显著降低.
- 激活SIRT2或过度表达BMAL1减轻了棕酸引起的损伤.
结论:
- 棕酸破坏BMAL1-NAD+-SIRT2通路,导致肝细胞受损.
- SIRT2是一种时钟控制的基因,在转录水平上由BMAL1调节.
- 激活BMAL1-NAD+-SIRT2轴显示出对脂毒性和炎症的肝保护作用.
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