Salvianolic acid B ameliorates lipopolysaccharide-induced inflammatory liver injury via deacetylation of NF-κB RelA

文献类型： 外文期刊

第一作者： Wang, Hao

作者： Wang, Hao;Lai, Chenhuan;Chen, Yanan;Wang, Hao;Lai, Chenhuan;Chen, Yanan;Wang, Hao;Zhang, Hao

作者机构：

关键词： Salvianolic acid B; Inflammatory liver injury; Lipopolysaccharide; Nuclear factor kappa B; Sirtuin 1

期刊名称：FOOD BIOSCIENCE （ 影响因子：5.9； 五年影响因子：6.1 ）

ISSN： 2212-4292

年卷期： 2025 年 68 卷

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收录情况： SCI

摘要： Liver diseases, ranging from simple fatty liver to viral hepatitis and cirrhosis, represent a major public health concern. Although the underlying mechanisms remain unclear, hepatic inflammation has emerged as a key factor driving disease progression. Here, we investigated the protection of salvianolic acid B (SAB) against lipopolysaccharide (LPS)-induced inflammatory liver injury, both in vivo in piglets and in vitro in AML12 cells. One hundred forty-four male weanling piglets were divided into three groups: non-challenged group, LPS-challenged group, and LPS-challenged group pretreated with SAB. Each group had eight replicates, with six pigs per replicate. After a 21-days feeding trial, piglets received either sterile saline or LPS via intraperitoneal injection. Six hours later, one piglet from each replicate was randomly selected for sample collection. Results showed that LPS challenge caused significant body weight loss and liver damage in piglets, as indicated by elevation in plasma aminotransferase levels, hepatic inflammatory cell infiltration, and hepatocyte apoptosis. In contrast, SAB reversed body weight loss, improved hepatic morphology, and decreased hepatic pro-inflammatory mediators and apoptosis in LPS-challenged piglets. Transcriptomic analysis revealed that SAB suppressed hepatic signaling pathways related to inflammation and apoptosis, including tumor necrosis factor, nuclear factor kappa B (NF kappa B), and viral protein interaction with cytokine and cytokine receptor in LPS-challenged piglets. Mechanistically, SAB protected against LPS-induced inflammation and apoptosis by facilitating the deacetylation of NF-kappa B RelA through sirtuin 1. These findings provide novel evidence supporting SAB as a potential therapeutic candidate for inflammatory liver disorders.

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