Ginsenoside RD prevents acute liver injury in mice by inhibiting STAT3-mediated NLRP3/GSDMD activation

IF 4.3 3区材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC

ACS Applied Electronic Materials Pub Date : 2024-08-28 DOI:10.1002/jbt.23825

Wenyan Li, Yun Kong, Caiqun Zhang

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Abstract

We investigated the role and mechanism of ginsenoside RD (GRD) in acute liver injury. Network pharmacology was used to analyze the correlations among GRD-liver injury-pyroptosis targets. A mouse model of acute liver injury was established by lipopolysaccharide + d-galactose（LPS + d/Gal). After pretreatment with GRD, the changes in mouse liver function were detected. The histopathological changes were assayed by hematoxylin and eosin and Masson staining, the tissue expressions of inflammatory cytokines were detected by enzyme-linked immunosorbent assay, and the protein expressions were assayed by immunohistochemical staining and Western blotting. Meanwhile, mechanism research was conducted using STAT3-knockout transgenic mice and STAT3-IN13, a STAT3 inhibitor. GRD inhibited liver injury, mitigated tissue inflammation, and suppressed STAT3-mediated pyroptosis in mice. After applying STAT3-knockout mouse model or STAT3-IN13, GRD did not further inhibit the liver injury. GRD can resist liver injury by inhibiting the STAT3-mediated pyroptosis, which is one of the hepatoprotective mechanisms of GRD.

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人参皂苷 RD 通过抑制 STAT3 介导的 NLRP3/GSDMD 激活，预防小鼠急性肝损伤。

我们研究了人参皂苷 RD（GRD）在急性肝损伤中的作用和机制。利用网络药理学分析了GRD-肝损伤-突变靶点之间的相关性。通过脂多糖+d-半乳糖（LPS+d/Gal）建立了小鼠急性肝损伤模型。使用GRD预处理后，检测小鼠肝功能的变化。组织病理学变化采用苏木精、伊红和马森染色法检测，炎症细胞因子的组织表达采用酶联免疫吸附法检测，蛋白质表达采用免疫组化染色法和 Western 印迹法检测。同时，利用 STAT3 基因敲除转基因小鼠和 STAT3 抑制剂 STAT3-IN13 进行了机理研究。结果表明，GRD能抑制小鼠肝损伤，减轻组织炎症反应，抑制STAT3介导的脓毒症。在应用 STAT3 基因敲除小鼠模型或 STAT3-IN13 后，GRD 没有进一步抑制肝损伤。GRD可以通过抑制STAT3介导的热蛋白沉积来抵抗肝损伤，这是GRD的保肝机制之一。

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来源期刊

ACS Applied Electronic Materials Multiple-

CiteScore

7.20

自引率

4.30%

发文量

567