Fig. 5

ADSC-CM decreased scar fibrosis through the p38/MAPK signaling pathway in HSFs in vitro. a, b To explore the underlying mechanism of the anti-fibrotic effect of ADSC-CM, the protein level p-p38 was measured by Western blotting in primary HSFs in different concentrations of ADSC-CM (10 %, 20 %, 40 %, and 80 % concentrations of diluted conditioned medium); graph shows the relative band density to total p38. c, d The protein level of p-p38, Col1, Col3, and α-SMA in HSFs stimulated with DMEM in the presence of SB203580. e, f Western blotting analysis for p-p38 in primary HSFs stimulated with 20 % and 80 % concentrations of ADSC-CM in the presence of SB203580; the histogram presents the p-p38/p38 ratio. g–j Protein levels of Col1, Col3, and α-SMA stimulated with 20 % and 80 % concentrations of ADSC-CM in the presence of SB203580; graph shows the relative band density to β-actin. k Immunoblot analysis of p-p38, Col1, Col3, and α-SMA when stimulated with SB203580 and/or anisomycin. The data are shown as mean ± SEM from three independent experiments (*P < 0.05; **P < 0.01). A anisomycin, ADSC-CM adipose tissue-derived stem cell-conditioned medium, Col1 collagen I, Col3 collagen III, DMEM Dulbecco’s modified Eagle medium, S SB203580, SMA smooth muscle actin