ArticleThe American journal of pathology2002
The combination of ischemic preconditioning and liver Bcl-2 overexpression is a suitable strategy to prevent liver and lung damage after hepatic ischemia-reperfusion.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- Effect of silibinin on the expression of MMP2, MMP3, MMP9 and TIMP2 in kidney and lung after hepatic ischemia/reperfusion injury in an experimental rat model.Acta cirurgica brasileira · 2021Article
- Data on Adiponectin from 2010 to 2020: Therapeutic Target and Prognostic Factor for Liver Diseases?International journal of molecular sciences · 2020Review
- Pretreatment with a Phosphodiesterase-3 Inhibitor, Milrinone, Reduces Hepatic Ischemia-Reperfusion Injury, Minimizing Pericentral Zone-Based Liver and Small Intestinal Injury in Rats.Annals of transplantation · 2020Article
- Lung matrix metalloproteinase activation following partial hepatic ischemia/reperfusion injury in rats.TheScientificWorldJournal · 2014Article
- Pathophysiology of acute kidney injury.Comprehensive Physiology · 2012Review
- Ischemic postconditioning attenuates liver warm ischemia-reperfusion injury through Akt-eNOS-NO-HIF pathway.Journal of biomedical science · 2011Article
- Impact of hypoxic hepatitis on mortality in the intensive care unit.Intensive care medicine · 2011Article
- Protective effect of intermittent clamping of the portal triad in the rat liver on liver ischemia-reperfusion injury.Hepatitis monthly · 2011Article
- Hypoxic hepatitis - epidemiology, pathophysiology and clinical management.Wiener klinische Wochenschrift · 2010Review
- Role of ischemic preconditioning in liver surgery and hepatic transplantation.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2009Review
- Protection against hepatocyte mitochondrial dysfunction delays fibrosis progression in mice.The American journal of pathology · 2009Article
- Hypoxic hepatitis: underlying conditions and risk factors for mortality in critically ill patients.Intensive care medicine · 2009Article
- Effects of ischemic preconditioning on cyclinD1 expression during early ischemic reperfusion in rats.World journal of gastroenterology · 2006Article
- Protective effects of tumor necrosis factor alpha antibody and ulinastatin on liver ischemic reperfusion in rats.World journal of gastroenterology · 2004Article
- Forever young: mechanisms of natural anoxia tolerance and potential links to longevity.Oxidative medicine and cellular longevityReview
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study evaluates the effectiveness of ischemic preconditioning and Bcl-2 overexpression against the liver and lung damage that follow hepatic ischemia-reperfusion and investigates the underlying protective mechanisms. Preconditioning and Bcl-2, respectively, reduced the increased tumor necrosis factor (TNF) and macrophage inflammatory protein-2 (MIP)-2 levels observed after hepatic reperfusion. Bcl-2 overexpression or anti-MIP-2 pretreatment seems to be more effective than preconditioning or anti-TNF pretreatment against inflammatory response, microcirculatory disorders, and subsequent hepatic ischemia-reperfusion injury. Furthermore, each one of these strategies individually was unable to completely inhibit hepatic injury. The combination of preconditioning and Bcl-2 overexpression as well as the combined anti-TNF and anti-MIP-2 pretreatment totally prevented hepatic injury, whereas the benefits of preconditioning and Bcl-2 were abolished by TNF and MIP-2. In contrast to preconditioning, Bcl-2 did not modify lung damage induced by hepatic reperfusion. This could be explained by the differential effect of both treatments on TNF release. Anti-TNF therapy or preconditioning, by reducing TNF release, reduced pulmonary inflammatory response, whereas the benefits of preconditioning on lung damage were abolished by TNF. Thus, the induction of both Bcl-2 overexpression in liver and preconditioning, as well as pharmacological strategies that simulated their benefits, such as anti-TNF and anti-MIP-2 therapies, could be new strategies aimed to reduce lung damage and inhibit the hepatic injury associated with hepatic ischemia-reperfusion.
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