Huatan Qushi Huoxue Formula for Metabolic Associated Fatty Liver Disease: Multi-Omics and Networ

02 Apr 20264 min read0 viewsJournal Feed

GIST

ObjectiveThis study aimed to evaluate the therapeutic effect of the traditional Chinese medicine compound Huatan Qushi Huoxue prescription (HQHF) on Metabolic Associated Fatty Liver Disease (MAFLD) and explore its underlying mechanisms through a multi-method approach.MethodsA high-fat diet-induced MAFLD mouse model was established to assess HQHF’s effects on liver pathology, biochemical markers, and oxidative stress. The bioactive components and potential targets of HQHF were identified through network pharmacology.

MAFLD-related signaling pathways were explored by integrating data from the Gene Expression Omnibus (GEO) database, followed by molecular docking analyses. For experimental validation, key inflammatory cytokines and proteins (Interleukin-6 (IL-6), Interleukin-1α (IL-1α), Interleukin-1β (IL-1β), Matrix Metallopeptidase 9 (MMP9), Chemokine Ligand 2 (CCL2), and Intercellular Adhesion Molecule 1 (ICAM1)) were measured using Enzyme-Linked Immunosorbent Assay (ELISA), immunohistochemistry (IHC), and immunofluorescence.ResultsHistopathological analysis showed that HQHF significantly alleviated liver steatosis and inflammatory cell infiltration.

Biochemical analysis indicated that HQHF reduced serum and liver triglyceride levels, serum total cholesterol, liver enzymes (Aspartate Aminotransferase, AST, and Alanine Aminotransferase, ALT), and malondialdehyde (MDA), while increasing glutathione (GSH) levels.

Clinical Editorial

Scope and objective

The study employs a multi-method framework to illuminate possible mechanisms.

The report characterizes the potential of Huatan Qushi Huoxue prescription (HQHF), a traditional Chinese medicine compound, as a therapeutic candidate for metabolic-associated fatty liver disease (MAFLD).

Experimental design and models

A high-fat diet–induced MAFLD mouse model was used to observe HQHF's impact on liver pathology, biochemical markers, and oxidative stress indices.
Parallel in silico analyses included network pharmacology to identify bioactive components and potential targets, and integration of GEO-derived MAFLD signaling data with molecular docking to infer pathway involvement.

Molecular targets and pathways

Network pharmacology mapped 33 bioactive constituents and 89 putative targets associated with HQHF.
Enrichment highlighted involvement of pathways such as MAPK, TLR, IL-17, and AGE-RAGE signaling.
Six core genes were emphasized: MMP9, IL1α, CCL2, IL1β, IL6, and ICAM1, suggesting a network of inflammation-related and matrix-remodeling processes.

Experimental readouts and key findings

Histology showed HQHF mitigated hepatic steatosis and inflammatory cell infiltration.
Biochemical assessments demonstrated reductions in serum and hepatic triglycerides, serum total cholesterol, and liver enzymes (AST and ALT), alongside decreased malondialdehyde (MDA) and increased glutathione (GSH) with HQHF treatment.
Experimental validation via ELISA, immunohistochemistry, and immunofluorescence indicated downregulation of targeted inflammatory mediators and adhesion molecules in HQHF-treated mice.
Molecular docking supported strong binding of principal HQHF constituents (notably quercetin and baicalin) to the identified core targets, aligning with observed experimental effects.

Context and implications

The integrated approach links lipid-lowering effects with anti-inflammatory activity, associating HQHF with modulation of multiple targets and pathways implicated in lipid metabolism and inflammatory signaling in MAFLD.
The evidence supports a multi-target, pathway-oriented mechanism rather than a single-molecule effect.

Limitations and uncertainties

The summary relies on the provided data; explicit study limitations or considerations regarding translational relevance were not detailed in the source material.