Fig. 2: Gut dysbiosis is normalized by HP.

a F/B ratio; (n = 10). b shannon and simpson index; (n = 10). c PcoA analysis among sham, MN+vehicle, MN + MMF and MN + HP (30 mg/kg) groups using the Bray–Curtis distance matrix; (n = 10). d taxonomic distribution on phylum level among different groups; (n = 10). e taxonomic distribution on genus level among different groups; (n = 10). f Top 30 differential genera caused by MN reversed by HP treatment; g The extent of KEGG pathway and module enrichment in the gut microbiota of the different experimental groups. The pathways disturbed by MN but restored by HP were shown in bold dark; (n = 10). h Concentration of acetic acid, propionic acid, and butyric acid in feces; (n = 6). i Concentration of indole and p-cresol in feces; j PcoA analysis of metabolite composition among sham, MN+vehicle, MN + MMF and MN + HP (30 mg/kg) groups; k KEGG pathways enriched by differential metabolites caused by MN; l Differential metabolites caused by gut dysbiosis of MN reversed by HP treatment; m KEGG pathways enriched by HP reversed metabolites in MN rats. Significant differences are indicated: #P < 0.05, ##P < 0.01, ###P < 0.001 versus sham group. *P < 0.05, **P < 0.01, versus vehicle-treated group by one-way ANOVA test, (n = 6). Bar graphs are means ± SD.