Curcumol inhibits keloid fibroblast proliferation and collagen synthesis through the ERK signaling pathway

OBJECTIVE To assess the effects of curcumol on the proliferation, apoptosis and collagen synthesis of keloid fibroblasts and explore the underlying mechanism. OBJECTIVE Keloid fibroblasts were treated with different concentrations of curcumol (10, 20, 40, 80 and 160 mg/L) or with 160 mg/L curcumol and 20 μmol/L ISO (an ERK signaling pathway activator). Western blotting was performed to detect the expression levels of proliferation-associated proteins (cyclin D1 and PCNA), fibrosis marker proteins (Col1A1, Col3A1 and α-SMA), apoptosis proteins (Bcl-2, Bax and cleaved caspase-3) and ERK signaling pathway proteins (p-ERK1/2, p-MEK and p-c-Raf) in the cells. MTT assay and flow cytometry were used to evaluate the proliferation and apoptosis rate of the treated cells, respectively. OBJECTIVE Curcumol at 10, 20, 40, 80 and 160 mg/L all reduced the protein expressions of cyclin D1, PCNA and Bcl-2, inhibited the expressions of fibrotic marker proteins Col1A1, Col3A1 and α-SMA, decreased the levels of ERK signaling pathway proteins p-ERK1/2, p-MEK and p-c-Raf, and increased the expressions of Bax and cleaved caspase-3 proteins (P < 0.05). Curcumol treatment at 160 mg/L obviously inhibited the proliferation and collagen synthesis, promoted cell apoptosis and inhibited the ERK signaling pathway in the keloid fibroblasts; treatment with ISO significantly reversed the effects of curcumol on the proliferation, apoptosis, collagen synthesis and ERK signal pathway of the cells. OBJECTIVE Curcumol regulates proliferation, apoptosis and collagen synthesis in keloid fibroblasts through the ERK signaling pathway.