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839通过抑制炎症和调节小鼠肠道微生物群来改善抗结核药物引起的肝损伤。

839 ameliorates anti-tuberculosis drugs-induced liver injury by suppressing inflammation and regulating gut microbiota in mice.

作者信息

Li Qiujuan, Wu Chenbing, Zhang Kangshuai, Zhou Ziyi, Li Jing, Bai Jie, Cao Jun, Shi Xiaoxia

机构信息

Department of Experimental Teaching Center of Public Health, Dalian Medical University, Dalian, China.

Department of Pathology and Forensic Medicine, Dalian Medical University, Dalian, China.

出版信息

Front Med (Lausanne). 2025 Apr 17;12:1538528. doi: 10.3389/fmed.2025.1538528. eCollection 2025.

Abstract

Anti-tuberculosis drug-induced liver injury (ATB-DILI), caused by first-line anti-tuberculosis (anti-TB) drugs, disrupts treatment and increases the risk of drug resistance. The gut microbiota and intestinal barrier integrity play key roles in ATB-DILI susceptibility through the liver-gut axis. Probiotics, such as 839 (BF839), have shown therapeutic potential in modulating gut microbiota and inflammatory responses. In this study, we investigated the protective effects of BF839 on ATB-DILI in a mouse model of HRZE-induced liver injury. BF839 administration significantly alleviated HRZE-induced liver injury by reducing ALT, AST, AKP, and MDA levels, enhancing SOD and GSH levels, and improving liver histopathology. These effects were associated with restored gut microbiota diversity, enhanced intestinal barrier function, and reduced inflammatory responses. Our findings suggest that BF839 may serve as a potential preventive strategy for ATB-DILI.

摘要

一线抗结核药物引起的抗结核药物性肝损伤(ATB-DILI)会干扰治疗并增加耐药风险。肠道微生物群和肠道屏障完整性通过肝肠轴在ATB-DILI易感性中起关键作用。益生菌,如839(BF839),已显示出调节肠道微生物群和炎症反应的治疗潜力。在本研究中,我们在HRZE诱导的肝损伤小鼠模型中研究了BF839对ATB-DILI的保护作用。给予BF839可通过降低ALT、AST、AKP和MDA水平、提高SOD和GSH水平以及改善肝脏组织病理学,显著减轻HRZE诱导的肝损伤。这些作用与恢复肠道微生物群多样性、增强肠道屏障功能和减少炎症反应有关。我们的研究结果表明,BF839可能是一种潜在的预防ATB-DILI的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a13/12043568/f949e3883f7e/fmed-12-1538528-g001.jpg

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