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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2011 Sep;58(3):263–271. doi: 10.1097/FJC.0b013e3182239eb7

Figure 1.

Figure 1

S17834 inhibits hydrogen peroxide (H2O2)- and TNFα-induced increases in p53-lysine 382 acetylation and cleaved caspase-3 in HAEC. Cells were treated with S17834 for 1 h prior to treating with H2O2 (A) or TNFα (B). p53 acetylation was evaluated 4 h after H2O2 and 6 h after TNFα. Caspase-3 acetylation was evaluated at 6 h. Representative immunoblots are shown above bar graphs summarizing results from 3 experiments. Total p53 was unchanged by H2O2, TNFα, or S17834. Total SirT1 was unchanged by TNFα or S17834 and α-actin, used as a loading control, was unchanged. The bar graphs indicate that H2O2 or TNFα significantly increased (*P<0.05) both p53 acetylation (black bar) and cleaved caspase-3 (striped bar), and S17834 significantly prevented the increase (†P<0.05). S17834 did not affect either p53 acetylation or caspase-3 cleavage in cells that were not treated with H2O2 or TNFα. Note that the bar graph in Figure 1B has two ordinates denoting p53 acetylation and caspase-3 cleavage separately.