Figure 7.

H₂S contributes to the cellular defense against acrolein-initiated oxidative cell injury. (A,B) effects of H₂S on acrolein-initiated cell death. HUVECs were exposed to 150 µM acrolein in the presence or absence of 2 mM BCA or 3 mM PAG (A), or 1 mM NaHS or 2 mM L-cysteine (L-Cys). The cell viability was determined by Calcein-AM/PI staining (A) and WST assay (B). Graph below the images in A and B are mean ± SE, n = 4; ** p < 0.01 versus control, ^## p < 0.01 versus acrolein alone. (C–I) effect of H₂S on acrolein-induced protein carbonylation, sulfenic acid formation, and P38 activation. HUVECs were exposed to 75 µM acrolein in the presence or absence of 2 mM BCA, 3 mM PAG, 1 mM NaHS or 2 mM L-cysteine for 1 h. Cellular lysates were assayed for protein carbonylation (C,D), sulfenic acid formation (E–G), and P38 activation (H,I). Equal loading of protein in each lane was confirmed either by re-probing the same blot with β-actin or through EZ blue staining.