乳酸脱氢酶
巨噬细胞极化
丹参
乳酸脱氢酶A
肝损伤
脂多糖
化学
四氯化碳
巨噬细胞
组蛋白
组蛋白H3
体内
分子生物学
生物化学
药理学
生物
体外
免疫学
医学
酶
病理
基因
四氯化碳
替代医学
生物技术
有机化学
中医药
作者
Shian Hu,Zehua Yang,Ling Li,Qingsheng Yan,Yanqiang Hu,Feng Zhou,Yang Tan,Gang Pei
出处
期刊:Molecules
[MDPI AG]
日期:2024-01-01
卷期号:29 (1): 236-236
标识
DOI:10.3390/molecules29010236
摘要
Salvianolic acid B (Sal B) is the primary water-soluble bioactive constituent derived from the roots of Salvia miltiorrhiza Bunge. This research was designed to reveal the potential mechanism of Sal B anti-liver injury from the perspective of macrophages. In our lipopolysaccharide-induced M1 macrophage model, Sal B showed a clear dose-dependent gradient of inhibition of the macrophage trend of the M1 type. Moreover, Sal B downregulated the expression of lactate dehydrogenase A (LDHA), while the overexpression of LDHA impaired Sal B’s effect of inhibiting the trend of macrophage M1 polarization. Additionally, this study revealed that Sal B exhibited inhibitory effects on the lactylation process of histone H3 lysine 18 (H3K18la). In a ChIP-qPCR analysis, Sal B was observed to drive a reduction in H3K18la levels in the promoter region of the LDHA, NLRP3, and IL-1β genes. Furthermore, our in vivo experiments showed that Sal B has a good effect on alleviating CCl4-induced liver injury. An examination of liver tissues and the Kupffer cells isolated from those tissues proved that Sal B affects the M1 polarization of macrophages and the level of histone lactylation. Together, our data reveal that Sal B has a potential mechanism of inhibiting the histone lactylation of macrophages by downregulating the level of LDHA in the treatment of liver injury.
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