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Mechanisms of Huatanqushihuoxue Formula (HQHF) in Ameliorating MAFLD 1 via Transcriptomic Analysis and Ferroptosis Regulation

ABSTRACT: Background: Metabolic dysfunction-associated fatty liver disease(MALD) is a prevalent condition with limited therapeutic options.Huatangushihuoxue Formula (HQHF) demonstrates efficacy against MAFLD, yet its broader clinical application is hindered by an unclear mechanism of action. Purpose:This study aimed to elucidate the therapeutic mechanisms and molecular targets of HQHF in MAFLD. Study design and Methods: MAFLD was induced in mice via a 26 high-fat diet (HFD). After HQHF intervention, systematic evaluations were conducted.Transcriptome analysis of liver tissues was performed, followed by Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of differentially expressed genes. Key targets were identified using Cytoscape.Experimental validations included protein immunoblotting, immunohistochemistry, quantitative PCR. and immunofluorescence.Finally, a preliminary analysis of the single-cell sequencing data was conducted. Results: Transcriptome analyses indicated that HQHF's therapeutic effects are centrally mediated through the regulation of oxidative stress and ferroptosis. Experimental validation confirmed that HQHF alleviates oxidative stress and inhibits ferroptosis to treat MALD. Furthermore, eight key target genes were identified: Tnfaip3, Cx3cll, ICAM-1, CCND1, MAPK13,VDAC2, ATF4, and c-Myc. HQHF was verified to regulate the expression of these genes, which are involved in MAFLD pathophysiology.

ORGANISM(S): Mus musculus

PROVIDER: GSE324134 | GEO | 2026/03/13

REPOSITORIES: GEO

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Project description:Sepsis-associated acute kidney injury (SA-AKI) is a critical condition characterized by high morbidity and mortality rates, particularly in intensive care settings. This study focuses on RP105, a pattern recognition receptor, exploring its role in moderating the mechanisms of oxidative stress and ferroptosis during SA-AKI, offering insights into its potential as a therapeutic target. SA-AKI model was established using RP105 knockout (KO) and wild-type (WT) mice through cecal ligation and puncture (CLP). Comprehensive evaluations included the assessment of ferroptosis markers and the expression levels of pro-inflammatory cytokines. RP105 expression was markedly reduced in the kidneys following CLP induction, correlating with worsened renal outcomes. Compared to the Sham group, RP105-/- mice displayed heightened renal damage, increased levels of oxidative stress markers, and enhanced lipid peroxidation. Notably, the deficiency of RP105 led to increased macrophage infiltration and a shift towards pro-inflammatory phenotypes, which further potentiated ferroptosis and exacerbated renal tissue damage. By influencing macrophage behavior and mitigating inflammatory responses. RP105 deficiency exacerbates macrophage-induced inflammation, oxidative stress, and ferroptosis, forming a vicious cycle that leads to more severe renal injury. These findings underscore the pivotal role of RP105 in mitigating oxidative stress and suppressing ferroptosis in the context of SA-AKI through regulation of the HO-1/SLC7A11/GPX4 axis. By preventing macrophage polarization toward a pro-inflammatory phenotype, RP105 alleviates inflammatory responses and tissue damage, highlighting its potential as a therapeutic target. In contrast, RP105 deficiency exacerbates macrophage-driven inflammation, oxidative stress, and ferroptosis, creating a vicious cycle that worsens kidney injury. Thus, RP105 emerges as a promising therapeutic candidate for mitigating sepsis-induced renal damage.

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Mechanisms of Huatanqushihuoxue Formula (HQHF) in Ameliorating MAFLD 1 via Transcriptomic Analysis and Ferroptosis Regulation

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