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. Author manuscript; available in PMC: 2010 Aug 15.
Published in final edited form as: Eur J Pharmacol. 2009 Jun 17;616(1-3):31–37. doi: 10.1016/j.ejphar.2009.06.012

Fig. 3.

Fig. 3

NDGA inhibits Smad2 phosphorylation induced by TGF-β treatment in Panc-1 cells. A. Panc-1 cells were pretreated with 40 µM NDGA or DMSO for one hour, followed by treatment with 10 ng/ml TGF-β for another hour. Phospho-Smad2 and Smad2 were tested by immunoblotting. TGF-β treatment induced increased Smad2 phosphorylation, and NDGA treatment inhibited this induction. There was no effect on total Smad2 level by any treatment. B. Panc-1 cells were treated with 40 µM NDGA or DMSO in the presence or absence of 10 ng/ml TGF-β for 3 days, with medium changed every two days. Phospho-Smad2 and Smad2 were tested by immunoblotting. TGF-β treatment increased Smad2 phosphorylation, and NDGA treatment inhibited this induction. There was no effect on total Smad2 level by any treatment. C. Panc-1 cells were pretreated with 100 µg/ml vitamin C, 30 µM caffeic acid, 30 µM 5,8,11-eicosatriynoic acid (ETI), 4 µM AG538, 4 µM picropodophyllin (PPP), or DMSO for one hour, followed by treatment with 10 ng/ml TGF-β for another hour. Phospho-Smad2 and Smad2 were tested by immunoblotting. There was no effect on Smad2 phosphorylation and total Smad2 level by any treatment.