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外源H₂S通过USP22/SIRT1轴减少由HepG2细胞中脂质混合引起的氧化应激

Xiaomeng Cui¹, Chengjun Li², Shuixiang He³

¹Department of Infectious Diseases, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, Shannxi, China.

Scientific reports

|July 2, 2025

概括

外源硫化 (H2S) 通过减少氧化应激和炎症来缓解非酒精性脂肪性肝病 (NAFLD). 它通过USP22通路稳定SIRT1蛋白水平来实现这一目标,保护肝细胞免受损伤.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
肝病学肝病学是一种肝病学.

背景情况:

氧化应激是非酒精性脂肪肝疾病 (NAFLD) 进展的关键驱动因素.
外源硫化 (H2S) 对NAFLD氧化应激的影响的确切机制尚不完全理解.
H2S在生理过程中扮演着不同的角色,包括抗氧化防御和炎症调节.

研究的目的:

在NAFLD细胞模型中阐明外源H2S调节氧化应激和炎症的特定机制.
研究USP22-SIRT1轴在调解H2S对肝细胞损伤的保护作用中的作用.

主要方法:

用脂聚糖 (LPS) 治疗HepG2细胞以诱导氧化应激和炎症,有或没有H2S捐赠者GYY4137.
评估了氧化应激标志物 (MDA,SOD,ROS) 和炎症性细胞因子 (TNF-α,IL-6) 的水平.
研究了抗氧化蛋白USP22和SIRT1的表达,并评估了USP22敲击对H2S疗效的影响.

主要成果:

外源H2S显著降低了MDA,ROS,TNF-α和IL-6水平,同时增加了LPS诱导的HepG2细胞中的SOD活性.
H2S治疗提高了USP22的表达,并抑制了SIRT1.1.的随处化介导的降解.
击败USP22减少了H2S对LPS诱导的氧化损伤和炎症的保护作用.

结论:

外源H2S在HepG2细胞中对NAFLD相关的氧化应激和炎症产生保护作用.
该机制涉及H2S诱导的USP22上调,后续抑制SIRT1无化和降解.
准USP22-SIRT1通路代表了管理NAFLD的潜在治疗策略.

关键词:

外源的H2S是一种外源的H2S GYY4137 时间时间时间脂质混合物脂质混合物氧化应激是一种氧化应激.一个SIRT1系统.美国P2222

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