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. Author manuscript; available in PMC: 2011 Apr 1.
Published in final edited form as: J Mol Cell Cardiol. 2010 Jun 8;49(4):625–638. doi: 10.1016/j.yjmcc.2010.05.014

Fig. 8.

Fig. 8

Fig. 8

Silencing G6PD attenuates BFT-induced protection on cardiomyocytes exposed to hypoxia under normal or high glucose. Bar graphs show G6PD activity (A), levels of activated caspase 3/7 (B), pVEGFR2 (C), pAKt (D), Pim-1(E) and Bcl-2 (F) in cultured adult cardiomyocytes after silencing G6PD. Cardiomyocytes cultured in normal (NG) or high glucose (HG) were transfected with siRNAG6PD (NGSiG and HGSiG) and subjected to hypoxia with 0.2% O2 for 18 h after treating the cells with BFT (NGBSiG and HGBSiG) or vehicle (NGVSiG or HGVSiG). Values are mean±standard deviation and expressed as U/min/mg of protein for G6PD activity, relative units (RLU) for caspase 3/7 activity and n-fold changes toward vehicle-treated NG (NGV) for pVEGFR2, pAkt, Pim-1 and Bcl-2.§P<0.01, §§P<0.001 and §§§P<0.0001 versus NG or HG; *P<0.01 and **P<0.001 versus vehicle-treated NG (NGV) or HG (HGV); #P<0.01 and ##P<0.001 versus BFT-treated NG (NGB) or HG (HGB); δP<0.01 and δδP<0.001 versus corresponding treatment between NG or HG cultured cells. Each experiment was repeated four times in triplicate except caspase 3/7 activity, which was performed in 6 wells per each condition and repeated 3 times.