Effect of celecoxib on proliferation, collagen expression, ERK1/2 and SMAD2/3 phosphorylation in NIH/3T3 fibroblasts

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• 作者：Fengfeng Li¹ ; Shen Liu¹ ; Yuanming Ouyang¹ ; Cunyi Fan ; ^{fancunyi888@hotmail.com} ; Ting Wang ; Changqing Zhang ; Bingfang Zeng ; Yimin Chai ; Xiang Wang
• 关键词：NIH/3T3 fibroblast ; Celecoxib ; ERK MAP kinases ; SMAD proteins
• 刊名：European Journal of Pharmacology
• 出版年：2012
• 出版时间：5 March, 2012
• 年：2012
• 卷：678
• 期：1-3
• 页码：1-5
• 全文大小：709 K

文摘

In the present study, the effects of celecoxib on proliferation, collagen expression, ERK1/2 and SMAD2/3 phosphorylation in NIH/3T3 fibroblasts were investigated. NIH/3T3 fibroblasts stimulated with fibroblast growth factor-2 (FGF-2) or transforming growth factor-¦Â1 (TGF-¦Â1) were examined in the presence of celecoxib. Proliferation was assessed by MTT assays; ERK1/2 expression and SMAD2/3 expression were assessed by quantitative RT-PCR and western blotting; ERK1/2 phosphorylation and SMAD2/3 phosphorylation were assessed by western blot analysis. The results indicated that celecoxib could suppress cell proliferation stimulated by FGF-2 (IC₅₀ FGF + group, 75 ¡À 1.9 ¦Ìmol/l) and TGF-¦Â1 (IC₅₀ TGF + group, 48 ¡À 1.4 ¦Ìmol/l), by inhibiting ERK1/2 phosphorylation but not ERK1/2 expression. Celecoxib also suppressed collagen expression (0.35-fold COL3 and 0.43-fold COL1 at 320 ¦Ìmol/l celecoxib relative to the untreated control after stimulation with TGF-¦Â1 for 3 h, P < 0.01), by inhibiting SMAD2/3 phosphorylation but not SMAD2/3 expression. The suppression of NIH/3T3 fibroblast proliferation and collagen expression upon stimulation by FGF-2 and TGF-¦Â1 is likely a result of the inhibition of ERK1/2 and SMAD2/3 phosphorylation by celecoxib.