Zhi-Hang Li’s research while affiliated with Changsha Medical University and other places

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Publications (1)

Effect of FAE on pathological changes of liver tissue. (A) Preparation of the hepatic fibrosis model and the drug intervention process. (B) Liver index. (C) HE and Masson staining. (D) Liver function via AST, ALT, T-Bil and TG expression. (E) Immunohistochemistry. n = 8, ** p ≤ 0.05 versus NOR; * p ≤ 0.05 versus MOD. C: →: necrocytosis; HE staining→: fat vacuole; Masson staining→: collagen deposition, E: →: necrocytosis; →: the express of α-SMA, Collagen1, NF-κB and TLR4, BD: p ≤ 0.05 represents a significant change. NOR, control group; MOD, model group; YZZ-H, high-dose FAE group; YZZ-M, medium-dose FAE group; YZZ-L, low-dose FAE group.
Effect of FAE on metabolites of hepatic fibrosis in mice. (A) PCA of quality control samples in positive ion mode. (B) PCA analysis of quality control samples in negative ion mode. (C) PLS-DA of differential metabolites between the model group and the blank group under positive ion mode. (D) PLS-DA of differential metabolites between the model group and the blank group under negative ion mode. (E) Volcano plot of the differential metabolites between the blank group and the model group under merge ion mode. (F) Volcano plot of the differential metabolites between the FAE group and the model group under merge ion mode. (G) Enrichment analysis of differential metabolite pathways between the FAE group and the model group. NOR, control group; MOD, model group; YZZ, high-dose FAE group.
The effect of FAE on gut microbiota in mice with hepatic fibrosis. (A) OTU expression in each group. (B) chao1 indexes. (C) Observed species index. (D) PLS-DA diagrams. (G) Linear discriminant analysis effect size analysis. (E,F) Relative abundance of gut microbiota in each group at the phylum level. n = 8, ** p ≤ 0.05 versus NOR; * p ≤ 0.05 versus MOD. NOR, control group; MOD, model group; YZZ, high dose FAE group.
Correlation analysis heatmap between the level of gut microbiota and differential metabolites in the liver.
Network pharmacological analysis chart. (A) Venn diagram of the intersection between component targets and disease targets. (B) PPI network. (C) GO enrichment analysis results. (D) Bubble diagram of the anti fibrotic pathway of FAE. (E) The molecular docking pattern with the highest total score.

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Combined metabolomics and 16S rDNA sequence analyses of the gut microbiome reveal the action mechanism of Fructus Akebiae against hepatic fibrosis
  • Article
  • Full-text available

February 2025

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5 Reads

Rong-Rong Wu

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Duo-Rui Nie

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Fang-Hui He

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Fei Xu

Objectives To explore the mechanism underlying the effect of Fructus Akebiae (FAE) against hepatic fibrosis in mice through combined network pharmacology, liver metabolomics, and 16S rDNA analyses of the gut microbiota. Methods In this study, we randomly divided mice into the control, model, FAE high-dose, FAE medium-dose, and FAE low-dose groups to analyze the pathological changes in the hepatic fibrosis and levels of the α-SMA, collagen 1, Nuclear Factor Kappa B (NF-κ B), Toll Like Receptor 4 (TLR4). The gut microbiota was analyzed through 16S rDNA sequencing analysis of liver metabolites using liquid chromatography-mass spectrometry. Furthermore, network pharmacology was used to determine the specific molecular regulation mechanism of FAE in hepatic fibrosis treatment. Results FAE treatment markedly improved the pathological changes in the hepatic fibrosis. Analysis revealed that FAE administration reversed the carbon tetrachloride (CCl4)-induced dysbiosis by increasing the abundance of Akkermansia and reducing that of Cyanobacteria. Additionally, metabolomic analysis showed that FAE treatment reversed the CCl4-induced metabolic disorders by regulating amino and nucleotide sugar metabolism. Furthermore, correlation analysis showed that Akkermansia and Verrucomicobiota were closely related to D-tolasaccharide and maltotetraose saccharide. Moreover, network pharmacology indicated that FAE might regulate the signaling pathway through the JUN/CASP3/NOS3/PTGS2/HSP90AA1 during treatment. Conclusion FAE may be a promising treatment for hepatic fibrosis, and its protective effects are associated with improvements in the microbiome and metabolic disorders.

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