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黑色素通过通过KEAP1/NRF2/HO-1通路抑制FFAs诱导的铁死来阻止MASLD的进展

Shuojiao Li^1,2, Peng Rao³, Wenxian Yu³

¹Department of Pharmacy, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.

Biomolecules & therapeutics

|August 18, 2025

概括

自由脂肪酸 (FFAs) 通过促进脂质积累和铁亡来驱动与代谢功能障碍相关的脂肪性肝病 (MASLD). 在MASLD模型中,通过减少氧化应激和铁亡,黑素治疗有效地减轻了肝损伤.

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
代谢疾病代谢疾病

背景情况:

代谢功能障碍相关的脂肪性肝病 (MASLD) 的特征是肝脏自由脂肪酸 (FFA) 积累,导致氧化应激和铁亡.
目前对MASLD的治疗选择有限,需要确定新的治疗点.

研究的目的:

调查FFAs和铁化在MASLD进展中的作用.
评估黑激素在缓解MASLD相关肝损伤方面的治疗潜力.

主要方法:

使用高脂肪饮食 (HFD) 和FFAs建立一个早期的MASLD模型 (NAFL).
对脂质代谢,肝细胞损伤,铁平衡和铁的综合分析.
评估黑素对脂质合成酶,铁调节,氧化应激以及KEAP1/NRF2/HO-1通路的影响.

主要成果:

HFD和FFAs治疗增加了脂质合成 (ACC1,FASN),肝脏脂质沉积,铁负荷和铁 (减少了GPX4).
氨酸的使用抑制了脂质合成,降低了肝脏脂质积累,缓解了铁失调,减少了肝损伤.
黑色素通过调节KEAP1/NRF2/HO-1通路来减弱铁亡,从而减少氧化应激.

结论:

黑色素有效地减轻MASLD的进展,通过抑制FFA诱导的氧化应激和ferroptosis.
黑色素显示出作为管理MASLD的治疗剂的潜力.
了解FFAs,铁恒温和铁的相互作用对于MASLD治疗策略至关重要.

关键词:

铁化是铁化的一种.自由脂肪酸是自由的脂肪酸.脂质过氧化过氧化黑色素是什么黑色素是什么黑色素是什么与代谢功能障碍相关的脂肪性肝病.

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