Hepatoprotective effects of Hovenia dulcis seeds against alcoholic liver injury and related mechanisms investigated via network pharmacology

Figure 1 Effects of Hovenia dulcis seeds on hepatic biomarkers in mice with alcoholic liver injury. A: Superoxide dismutase; B: Catalase; C: Glutathione; D: Malondialdehyde; E: Hepatic triglyceride. ^aP < 0.05, ^bP < 0.01 vs control group; ^cP < 0.05, ^dP < 0.01 vs model group. Error bars: standard deviations (n = 8). H. dulcis: Hovenia dulcis; SOD: Superoxide dismutase; CAT: Catalase; GSH: Glutathione; MDA: Malondialdehyde; hTG: Hepatic triglyceride.

Figure 2 Histopathological changes (magnified × 400 times, stained by hematoxylin and eosin). A: Control group; B: Model group; C: Hovenia dulcis seed group. Scale bar: 50 μm; Oval: Area with lipid droplets; Arrow: Inflammatory cells.

Figure 3 Protein–protein interaction network and node degrees. A: Interaction of 173 common target proteins; B: Thirty targets with the highest node degrees.

Figure 4 Complex interaction network between targets, the eligible ingredients, and alcoholic liver disease. A: Perlolyrine; B: β-sitosterol; C: Kaempferol; D: Naringenin; E: Stigmasterol; F: Quercetin. ALD: Alcoholic liver disease; H. dulcis: Hovenia dulcis.

Figure 5 Top 20 enriched biological processes from gene ontology analysis. FDR: False discovery rate.

Figure 6 Top 20 enriched pathways from Kyoto Encyclopedia of Genes and Genomes analysis. FDR: False discovery rate.