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首页|期刊导航|集成技术|6H2单克隆抗体靶向脂肪酸结合蛋白减轻脂多糖诱导脓毒症的全身炎症和器官损伤

6H2单克隆抗体靶向脂肪酸结合蛋白减轻脂多糖诱导脓毒症的全身炎症和器官损伤

Muhammad Mustapha IBRAHIM 方程

集成技术2026,Vol.15Issue(1):56-66,11.
集成技术2026,Vol.15Issue(1):56-66,11.DOI:10.12146/j.issn.2095-3135.20250724001

6H2单克隆抗体靶向脂肪酸结合蛋白减轻脂多糖诱导脓毒症的全身炎症和器官损伤

Targeting Fatty Acid-binding Protein with 6H2 Monoclonal Antibody Mitigates Systemic Inflammation and Organ Damage in LPS-induced Sepsis

Muhammad Mustapha IBRAHIM 1方程1

作者信息

  • 1. 中国科学院深圳先进技术研究院 深圳 518055||中国科学院大学 北京 100049
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摘要

Abstract

Dysregulated inflammation and multi-organ failure are hallmarks of sepsis,a potentially fatal illness for which there are currently no effective treatments.Fatty acid-binding protein(A-FABP)has been identified in recent research as a crucial mediator of the inflammatory pathways underlying sepsis.In this study,we used a murine model of lipopolysaccharide(LPS)-induced endotoxemia to assess the therapeutic potential of 6H2,a monoclonal antibody that targets A-FABP.In comparison to untreated septic mice,6H2 treatment significantly increased survival rates,decreased histopathological damage in the liver,lungs,kidneys,and heart,and reduced systemic inflammation.According to biochemical analyses,6H2 treatment decreased circulating levels of A-FABP,and this was associated with a reduction in inflammatory markers.These results indicate that A-FABP inhibition is a potentially effective treatment approach for sepsis,with 6H2 demonstrating strong therapeutic efficacy.

关键词

脓毒症/脂肪酸结合蛋白/脂多糖

Key words

sepsis/fatty acid-binding protein/LPS

分类

生物科学

引用本文复制引用

Muhammad Mustapha IBRAHIM,方程..6H2单克隆抗体靶向脂肪酸结合蛋白减轻脂多糖诱导脓毒症的全身炎症和器官损伤[J].集成技术,2026,15(1):56-66,11.

基金项目

国家自然科学基金项目(31900704) (31900704)

广东省基础与应用基础研究基金项目(2023A1515010467) (2023A1515010467)

深圳市科技创新委员会项目(JCYJ20230807140721043) This work is supported by National Natural Science Foundation of China(31900704),Guangdong Basic and Applied Basic Research Foundation(2023A1515010467),Science Technology and Innovation Commission of Shenzhen Municipality(JCYJ20230807140721043) (JCYJ20230807140721043)

集成技术

2095-3135

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