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. 2013 Sep 16;36(4):376–384. doi: 10.1007/s10059-013-0210-y

Fig. 3.

Fig. 3.

SAM inhibits endothelial apoptosis by inducing HO-1. (A) Representative Western blots of UCP2, MnSOD, Gpx1 and NQO1 under the experimental conditions described in Fig. 2A. (B) Concentration-dependent increase in HO-1 mRNA and protein expression by SAM. (C) Effect of SAM and LA on HO-1 expression. HAECs were pretreated for 1 h with SAM (200 μM) and then exposed to LA (300 μM) for 6 h. (D) Effect of SAM on intracellular ROS levels. Intracellular ROS production was determined by measuring the intensity of DCF. (E) Representative Western blot and quantification showing suppression of HO-1 protein expression by HO-1 siRNA. (F) HO-1 knockdown with siRNA opposes the effects of SAM to prevent cell apoptosis. HAECs were transfected with control siRNA or siRNA targeting HO-1, pretreated with SAM (200 uM) for 1 h and then exposed to LA (300 μM) for 6 h. Cell apoptosis was measured by a cell death ELISA kit. Data are presented as the mean ± SEM (n = 5). *P < 0.05 vs untreated cell, #P < 0.05 vs LA-treated cells, **P < 0.05 vs control siRNA-transfected cells.