Fig. 6

hADMSCs-Exo inhibited HSCs activation and liver fibrosis through PI3K/AKT/mTOR signaling pathway. A Heatmap of differential expression analysis of RNA-sequencing data from LFG, REG and hADMSCs-Exo. B Venn diagram of LFG vs REG, LFG vs hADMSCs-Exo and REG vs hADMSCs-Exo. C GO analysis results of the DEGs between REG and hADMSCs-Exo, including cell component (CC), molecular function (MF) and biological process (BP). Red represents CC, green represents MF, blue represents BP. D The top 10 significant GO terms of DEGs. E KEGG analysis of significant pathway of DEGs. F Volcano plot and significantly DEGs in PI3K/AKT pathway. Red represents up-regulated, blue represents down-regulated genes. G The mRNA levels of significantly DEGs in PI3K/AKT pathway were determined by qRT–PCR. H Fibronectin and AKT protein levels in LX-2 or treated with pbs, hADMSCs-Exo in the presence of TGF-β1 (10 ng/ml) for 24 h were measured by immunofluorescence staining. I Western blot assay for AKT, mTOR and phosphorylated and total PI3K p85 and PI3K p110 in mouse liver issue. J Quantification of AKT and mTOR by qRT–PCR. K The expression level of AKT, mTOR and phosphorylated and total PI3K p85 and PI3K p110 after HSCs were incubated with hADMSCs-Exo. LFG, liver fibrosis group, REG, regression group. Data are presented as means with SEM (n = 3 independent experiments). ns, not significant, *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001