Ching Shum Pills alleviates non-alcoholic fatty liver disease in mice by ameliorating lipid metabolism disorders
10.12122/j.issn.1673-4254.2025.09.04
- VernacularTitle:清心牛黄丸通过改善脂质代谢紊乱缓解小鼠非酒精性脂肪性肝病
- Author:
Biyun LUO
1
;
Xin YI
;
Yijing CAI
;
Shiqing ZHANG
;
Peng WANG
;
Tong LI
;
Pingzheng ZHOU
Author Information
1. 南方医科大学药学院,广东 广州 510515;南方医科大学第五附属医院药学部,广东 广州 510925
- Collective Name:YUNG Ken Kin Lam
- Publication Type:Journal Article
- Keywords:
non-alcoholic fatty liver disease;
Ching Shum Pills;
quercetin;
lipid metabolism;
liver function
- From:
Journal of Southern Medical University
2025;45(9):1840-1849
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of Ching Shum Pills(CSP)for alleviating non-alcoholic fatty liver disease(NAFLD)and the underlying mechanism.Methods In a mouse model of NAFLD,the therapeutic effect of CSP was evaluated by measuring serum glucose,lipid profiles(TC,TG,LDL-C,HDL-C),and hepatic function markers.Network pharmacology was employed to identify active compounds in CSP and their targets using TCMSP,HERB,SwissTargetPrediction,GeneCards,OMIM,and DisGeNET.Protein-protein interaction(PPI)networks,Gene Ontology(GO),and KEGG pathway analyses were conducted.Molecular docking(AutoDock Vina)was used to assess the compound-target binding affinities.Quantitative real-time PCR(qRT-PCR)was used to validate the mRNA expressions of the core genes in the liver tissue of the mouse models.Results In the mouse model of NAFLD,treatment with CSP significantly reduced body weight gain and serum TG levels of the mice,and high-dose CSP treatment resulted in obvious reduction of ALT levels and hepatic fat accumulation.Network pharmacology analysis identified quercetin and 2-monolinolenin as the key bioactives in CSP,which target TNF,AKT1,IL6,TP53,and ALB.Docking simulations suggested strong binding between the two core compounds and their target proteins.The results of qRT-PCR showed that high-fat diet induced significant downregulation of Tp53,Cpt1,and Ppara expressions in mice,which was effectively reversed by CSP treatment.Conclusion CSP can improve lipid metabolism disorders in NAFLD mice through a regulatory mechanism involving multiple targets and pathways to reduce liver fat accumulation and protect liver function.The key components in CSP such as quercetin and linolenic acid monoacylglycerol may participate in the regulation of such metabolic processes as fatty acid oxidation by targeting TP53.
