Fig. 5
hUCMSC-EVs inhibited the activation of HSCs. a Distribution of DIR-labeled hUCMSC-EVs in S. japonicum-infected mice (left, 28-day infection) and in infected mice liver (right, DiR-labeled EVs treatment 2 days) after tail vein administration. Control, uninfected mice injected with PBS; EVs, infected mice administrated DiR-labeled hUCMSC-EVs. b Immunohistochemical staining and c western blotting results of α-SMA in liver sections from infected mice after 56-day infection. EVs, hUCMSC-EVs. Real-time PCR analysis of d α-SMA, e collagen 1, and f collagen 3 in the liver samples from infected mice after 56-day infection. *P < 0.05, compared with the PBS group. g LX-2 cells (5 × 103) were incubated in the presence or absence of hUCMSC-EVs for 24 h or 48 h. The cell viability was determined via the CCK8 assay. *P < 0.05; **P < 0.01; ***P < 0.001, compared with the 0 group. h LX-2 cells (5 × 103) were incubated in the presence or absence of hUCMSC-EVs (2 × 109/ml) for 48 h. The cell proliferation was measured using EdU cell proliferation assay. Real-time PCR analysis for TGF-β1-induced or hUCMSC-EVs reversed fibrosis-related i α-SMA, collagen 1 and collagen 3 products. *P < 0.05; **P < 0.01; ***P < 0.001, compared with the control or TGF-β1 treatment (20 ng/mL) group