Abstract
In vitro studies (1–3) have found the molecular signaling pathways of heme oxygenase (HO)-1 induction included MAPKs, Nrf2, and Bach1. However, the cellular mechanism of HO-1 induction in the target tissue (liver) by remote ischemic preconditioning (limb) is still under investigation. It has been proposed that either neurogenic and/or humoral factors were responsible for the induction of HO-1. The blocking assays were the commonly used methods to prove these theories. For example, ganglion blockers (4, 5) or mitochondria KATP channel blocker (6) have been shown to inhibit the protective effect of remote preconditioning. In our study, though we demonstrated the HO-1 was not induced in the peripheral lymphocytes but in the liver, we did not find the exact mechanism of remote HO-1 induction. Kanoria et al. (7) has indicated nitric oxide (NO) as an important mediator of the protective effect of limb remote ischemic preconditioning (RIPC). Is it possible that NO also is an important inducer of HO-1 expression? Choi et al. had shown that NO donor upregulated HO-1 expression in hepatocyte cultures (8, 9). The endothelium of limb vessels might produce NO derivatives in the process of limb ischemia-reperfusion. The study of Kanoria et al. (7) showed increased nitrate/nitrite levels in hepatic vein and systemic arterial plasma after RIPC. However, there existed another puzzle that how the short-lived NO derivatives transfer signals to induce HO-1 in remote liver. Of course, remote hepatic HO-1 induction might simply reflect secondary liver ischemic stress originating from limb ischemia-reperfusion. To solve this problem, we have to investigate the perfusion dynamics of liver during limb ischemia-reperfusion. I-Rue Lai King-Jen Chang Department of Surgery National Taiwan University Hospital National Taiwan University College of Medicine Taipei, Taiwan Chau-Fong Chen Department of Physiology National Taiwan University College of Medicine Taipei, Taiwan
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
