W Yuan1, H Sun1, L Yu1, J Wang2. 1. Department of Plastic Surgery, Shenzhen People's Hospital, Shenzhen 518020, China. 2. Collaborative Innovation Center of Translational Medicine, Shenzhen People's Hospital, Shenzhen 518020, China.
Abstract
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.
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.