This study aimed to investigate whether celecoxib suppresses fibroblast proliferation and collagen expression by inhibiting extracellular signal-regulated kinase 1/2 (ERK1/2) and SMAD2/3 phosphorylation. Celecoxib was added to NIH/3T3 fibroblasts stimulated by fibroblast growth factor-2 (FGF-2) or transforming growth factor-β1 (TGF‑β1). NIH/3T3 fibroblast proliferation and viability were assessed by MTT assays; ERK1/2 expression and SMAD2/3 expression were assessed by quantitative RT-PCR and Western blot analysis. The results indicated that celecoxib suppressed cell proliferation (IC50 FGF+ group, 75±1.9 µmol/l) stimulated by FGF-2, and also inhibited cell viability (IC50 FGF- group, 252±2.3 µmol/l) by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. In addition, celecoxib treatment led to the apoptosis of NIH/3T3 fibroblasts (IC50 FGF- group, 35±1.4 µmol/l). Celecoxib also suppressed collagen expression (0.35‑fold COL3 and 0.43‑fold COL1 with 320 µmol/l celecoxib relative to the untreated group following stimulation for 3 h, p<0.01) when stimulated by TGF‑β1, by inhibiting SMAD2/3 phosphorylation but not SMAD2/3 expression. Celecoxib is capable of inhibiting ERK1/2 and SMAD2/3 phosphorylation, which is responsible for NIH/3T3 fibroblast proliferation and collagen expression.

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