Acetylcorynoline alleviates acute liver injury via inhibiting TLR4/JNK/ NF-KB pathway Based on RNA-seq and molecular docking in vivo and in vitro

被引：0

作者：

Fu, Jun ^{[1
,2
]}

Zhang, Zhenxu ^{[1
,2
]}

Zhao, Yaning ^{[1
,2
]}

Li, Xin ^{[1
,2
]}

Jiang, Cuihua ^{[1
,2
]}

He, Haoran ^{[1
,2
]}

Huo, Jiege ^{[1
,3
]}

Xiao, Qi ^{[1
]}

Wu, Jie ^{[1
]}

Zhu, Fenxia ^{[1
,2
]}

Chen, Jiaquan ^{[4
]}

机构：

[1] Nanjing Univ Chinese Med, Affiliated Hosp Integrated Tradit Chinese & Wester, Nanjing 210028, Peoples R China

[2] Jiangsu Prov Acad Tradit Chinese Med, Key Lab New Drug Delivery Syst Chinese Mat Med, Nanjing 210028, Peoples R China

[3] Jiangsu Clin Innovat Ctr Digest Canc Tradit Chines, Nanjing 210028, Peoples R China

[4] China Pharmaceut Univ, Sch Sci, Dept Chem, Nanjing 211198, Peoples R China

来源：

INTERNATIONAL IMMUNOPHARMACOLOGY | 2024年 / 143卷

关键词：

Acetylcorynoline; Acute liver injury; Liver inflammation; RNA-Seq; Molecular docking; KAPPA-B; STIMULATED RAW264.7; GENE-EXPRESSION; FAILURE; CELLS;

D O I：

10.1016/j.intimp.2024.113550

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Acute liver injury is characterized by massive inflammatory cell infiltration, destruction of liver structure and abnormalities in liver function. Acetylcorynoline (AC) is one of the main chemical components of Corydalis bungeana Turcz. which has been shown to have a protective effect against acute liver injury. However, Whether AC is protective against acute liver injury remains unclear. This study aimed to explore the protective mechanism of AC against acute liver injury from in vivo as well as experiments in vitro. In experimental in vivo studies, AC pretreatment reduced the serum levels of ALT and AST and inhibited the expression of inflammatory factors in the liver of LPS/D-GalN-induced mice and alcohol liver disease mice. RNA-sequencing and molecular docking were used to predict that AC exerts its anti-inflammatory effects through the Toll-like receptor signaling pathway. Using RT-qPCR and Western blotting to detect expression levels of key genes and nodal proteins of the Toll-like receptor signaling pathway, AC was found to inhibit the phosphorylation of nuclear factor-kappaB (NFKB) and c-Jun amino-terminal kinase (JNK). This finding was validated in cellular experiments. In conclusion, AC exerts its anti-hepatic injury effect by suppressing inflammation through inhibition of the TLR4/JNK/NF-KB pathway.

引用

页数：13