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
- Author:
Biyun LUO
1
;
Xin YI
1
;
Yijing CAI
1
;
Shiqing ZHANG
2
;
Peng WANG
3
;
Tong LI
3
;
Ken Kin Lam YUNG
4
;
Pingzheng ZHOU
1
Author Information
1. School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China.
2. College of Pharmacy, Jinan University, Guangzhou 510632, China.
3. Department of Pharmacy, Fifth Affiliated Hospital of Southern Medical University, Guangzhou 510925, China.
4. Department of Science and Environmental Studies, the Education University of Hong Kong, Hong Kong 999077, China.
- Publication Type:Journal Article
- Keywords:
Ching Shum Pills;
lipid metabolism;
liver function;
non-alcoholic fatty liver disease;
quercetin
- MeSH:
Animals;
Non-alcoholic Fatty Liver Disease/drug therapy*;
Mice;
Drugs, Chinese Herbal/pharmacology*;
Lipid Metabolism/drug effects*;
Molecular Docking Simulation;
Disease Models, Animal;
Liver/metabolism*;
Male;
Lipid Metabolism Disorders/drug therapy*;
PPAR alpha/metabolism*;
Mice, Inbred C57BL;
Network Pharmacology
- From:
Journal of Southern Medical University
2025;45(9):1840-1849
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES: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.
CONCLUSIONS: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.
