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纳西克拉辛通过ESR1/S100A11轴减轻与败血症相关的急性损伤

Liping Yin^1,2, Xiaofei Huang^1,2, Beibei Zhang^1,2

¹Department of Emergency and Critical Care Medicine, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210028, People's Republic of China.

Functional & integrative genomics

|January 14, 2025

概括

纳西克拉辛 (Ncs) 通过减少炎症和细胞损伤,防止与败血症相关的急性损伤 (SA-AKI). 它通过抑制ESR1/S100A11通路而起作用,为SA-AKI提供了一个新的治疗策略.

科学领域:

生物化学生物化学
分子生物学分子生物学
腎臟病學 (nephrology) 是一種神經病學.

背景情况:

败血症相关的急性损伤 (SA-AKI) 是败血症的一个关键并发症.
纳西克拉辛 (Ncs) 具有抗氧化特性,具有潜在的治疗应用.
了解SA-AKI中Ncs的保护机制对于开发向治疗至关重要.

研究的目的:

调查纳西克拉辛 (Ncs) 对败血症相关急性损伤 (SA-AKI) 的保护作用.
阐明Ncs在SA-AKI中的治疗作用背后的分子机制.
探索ESR1/S100A11信号通路在Ncs介导保护中的作用.

主要方法:

在小鼠中,SA-AKI通过结和刺穿诱导,然后进行Ncs预处理.
人类脏微血管内皮细胞 (RMEC) 用LPS进行刺激,并用Ncs.治疗.
通过基因/蛋白质表达分析,酶活性测定和细胞亡评估来评估分子机制.

主要成果:

在SA-AKI小鼠中,Ncs治疗减轻了组织损伤,减少了血清损伤标志物和促炎细胞因子.
在体外,Ncs增强了内皮细胞完整性标记物 (ZO-1,VE-cadherin,CD31),抗氧化酶活性 (SOD,GSH-Px,CAT),并减少了亡.
Ncs抑制了S100A11的ESR1转录;沉默S100A11扭转了ESR1过度表达的有害影响.

结论:

纳西克拉辛 (Ncs) 通过减轻损伤和炎症来改善败血症相关的急性损伤 (SA-AKI).
通过抑制ESR1/S100A11信号通路来介导Ncs的保护作用.
Ncs代表了SA-AKI的一个有前途的治疗剂,提供了一个新的研究视角.

关键词:

在ESR1中使用ESR1.纳西克拉西因是一种毒品.脏微血管内皮细胞是什么?在S100A1111中使用.与败血症相关的急性损伤

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