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通过激活库弗细胞,CXCL5促进了乙氨基诱导的肝毒性

Kexin Qiu^1,2, Yan Pan^1,2, Weizhi Huang^1,2

¹Department of Pathology and Institute of Oncology, The School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350122, China.

International journal of molecular sciences

|August 12, 2023

概括

通过激活Kupffer细胞 (KCs),CXC动机化学联体5 (CXCL5) 通过激活乙氨基 (APAP) 诱导的肝损伤. 中和CXCL5减少炎症和肝损伤,突出其在APAP肝毒性中的作用.

科学领域:

肝病学肝病学是一种肝病学.
免疫学免疫学免疫学
毒理学毒理学毒理学

背景情况:

库弗尔细胞 (KCs) 是乙氨基 (APAP) 诱导的急性肝损伤 (ALI) 的核心.
CXC动机化学因子连接体5 (CXCL5) 是一种促炎媒介,涉及各种炎症状况.

研究的目的:

研究CXCL5在KC激活中的作用及其对APAP诱导的肝毒性贡献.
评估在APAP诱导的ALI中抗CXCL5抗体的治疗潜力.

主要方法:

一个在体内小鼠模型的APAP诱导的ALI用抗CXCL5单克隆抗体 (mAb) 治疗.
肝损伤的生物化学和组织学评估.
在体外研究中,使用与KC共同培养的原发性肝细胞和用重组小鼠CXCL5或脂聚糖 (LPS) 的刺激.

主要成果:

在APAP诱导的受伤肝脏中,CXCL5表达显著升高.
抗CXCL5 mAb治疗减轻了APAP诱导的ALI,减少了肝细胞死亡和炎症,而不会影响APAP代谢.
在体外,CXCL5在共同培养的肝细胞和KC中增强了APAP诱导的毒性,而抗CXCL5 mAb在KC中减少了LPS诱导的炎症性细胞因子的产生.

结论:

CXCL5刺激KCs产生炎症媒介,加剧APAP诱导的肝毒性.
对CXCL5的中和提供了一种潜在的治疗策略,通过减少KC介导的炎症来治疗APAP诱导的ALI.

关键词:

在 APAP APAP 里面.在CXCL5中,CXCL5是CXCL5的前身.KCs 是一个 KC.肝细胞肝细胞肝细胞这是一种炎症炎症炎症炎症.

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