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. Author manuscript; available in PMC: 2016 Jan 22.
Published in final edited form as: Methods Enzymol. 2015 Jan 10;555:93–125. doi: 10.1016/bs.mie.2014.11.022

Figure 4.

Figure 4

Signaling mechanisms invoked by antecedent preconditioning with H2S donors 24 h prior to ischemia/reperfusion. Entrance into a protected state that limits postischemic leukocyte/endothelial cell adhesive interacts is triggered by an eNOS-derived NO-, p38 MAPK-, BKCa- and KATP-channel-dependent mechanism that is activated during the first hour after H2S donor administration. These triggering events activate as yet unknown obligatory downstream signaling mediators to promote increased expression and activity of heme oxygenase-1 (HO-1) between 8 and 24 h later. The enzymatic activity of HO-1 generates the anti-adhesive gasotransmitter carbon monoxide (CO) as well as the powerful antioxidants bilirubin and secondarily derived biliverdin, which act in concert to prevent postischemic leukocyte trafficking and neutrophil-dependent parenchymal cell injury.