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巨细胞中SIRT1不足会在痕形成过程中促进氧化应激和炎症

Ting He¹, Xiaozhi Bai¹, Yan Li¹

¹Department of Burns and Cutaneous Surgery, Xijing Hospital, Air Force Medical University, 127 Changle West Road, Xi'an, Shaanxi, 710032, China.

Journal of molecular medicine (Berlin, Germany)

|September 14, 2023

概括

巨细胞中的Sirtuin 1 (SIRT1) 对于伤口愈合至关重要. 缺乏SIRT1会通过增加氧化应激和激活NF-κB通路,加剧炎症和痕.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
伤口治愈研究研究伤口治愈研究

背景情况:

巨细胞的两极分化和激活是伤口愈合和痕形成的关键.
赛尔图因1 (SIRT1) 影响巨细胞的行为,但其在痕形成中的确切作用尚不清楚.

研究的目的:

研究SIRT1在皮肤伤口愈合和痕发育期间巨细胞功能中的特定作用.
阐明SIRT1,氧化应激和痕中的炎症之间的分子机制.

主要方法:

已确定的皮肤切口和LPS诱导的炎症小鼠模型.
在组织和巨细胞中检测到SIRT1表达.
利用SIRT1缺乏的巨细胞进行基于TMT的定量蛋白质组分析.
评估了活性氧物种 (ROS) 生产,NOX2,Nrf2和NF-κB通路的激活.

主要成果:

在痕组织中,SIRT1的表达被抑制,但在痕组织内的巨细胞中增加.
巨细胞特异性SIRT1缺乏会加剧炎症并促进痕.
蛋白质组分析揭示了NADH和氧化还原酶活动的差异表达.
抑制SIRT1加剧了ROS的产生和NOX2水平,同时抑制了Nrf2通路 (Nqo-1,HO-1),并激活了NF-κB通路.

结论:

在痕形成期间,巨细胞中SIRT1升高不足会导致过度激活的氧化应激和NF-κB信号,促进炎症和痕形成.
在巨细胞中提高SIRT1水平,为痕缓解提供了潜在的治疗策略.

关键词:

过度缩的痕过度缩的痕炎症炎症是一种炎症.巨细胞是一个巨细胞.氧化应激是一种氧化应激.一个SIRT1系统.伤口愈合伤口愈合

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