Bufalin and lycorine potently and specifically repress fibrotic responses in human cardiac fibroblasts (HCFs).
A, Filtering strategy, followed by in vitro and in vivo pipeline of analysis, uncovers antifibrotic lead compounds bufalin and lycorine. B, Functional screen of 480 naturally derived substances in vitro yielding natural compounds inhibiting the proliferation of HCFs. The cells were incubated for 24 hours as indicated, and proliferation of HCFs was measured by BrdU-ELISA. Fifteen candidates inhibiting the fibroblast proliferation fold change (FC) ≥75% are highlighted by the red rectangle. C, Dose-dependent inhibitory effects of bufalin, gitoxigenin, lycorine, anisomycin, and geldanamycin on proliferation of HCFs. The cells were incubated for 24 hours as indicated, and the proliferation of HCFs was measured by BrdU-ELISA (1-way ANOVA, Dunnett multiple-comparisons test, n=4-6). D, Positively validated hits do not induce cell death in HCFs. Cells were treated with respective compounds for 24 hours as indicated and subjected to fluorescence-activated cell sorter analysis after annexin-7AAD staining (unpaired t test, n=3). E, Dose-dependent inhibitory effects of bufalin and lycorine on proliferation of HCFs are fibroblast specific, as evidenced by no impact of the same concentrations of respective substances on the proliferation of the cardiomyocyte cell line HL-1. Cells were treated with the compounds for 24 hours as indicated, and proliferation of HL-1 cells was measured by BrdU-ELISA (1-way ANOVA, Dunnett multiple-comparisons test, n=3). F, Bufalin and, to a lesser extent, lycorine decrease expression levels of collagen type I, α1 (COL1A1) in HCFs shown in a representative Western blot. Cells were treated with respective substances for 24 hours as indicated, lysed, and analyzed for COL1A1 protein levels (normalized to GAPDH; unpaired t test). All values from C through F are presented as mean±SEM. DMSO indicates dimethyl sulfoxide; and ns, not significant. *P<0.05, **P<0.01, ***P<0.001, #P=0.265.