Postconditioning ameliorates lipid peroxidation in liver ischemia-reperfusion injury in rats.

PURPOSE Liver ischemia-reperfusion injury is a phenomenon presents in events like liver resections and transplantation. The restoration of blood flow may leads to local and systemic injury. Several techniques have been developed in order to avoid or ameliorate ischemia-reperfusion injury in clinical situations. The application of a stutter reperfusion after the ischemic event (postconditioning) could alters the hydrodynamics and stimulates endogenous mechanisms that attenuate the reperfusion injury. The present study was designed to evaluate the potential protective effect of postconditioning in a model of ischemia-reperfusion in rats. METHODS Hepatic anterior pedicle of median and left anterolateral segments were exposed and clamped for 1 hour. Two hours later, clamp was released in two different ways: Control Group (n=7): clamp was release straightforward; Postconditioning Group (n=7): clamp was released intermittently. Lipid peroxidation (malondialdehyde) and expression of the glutathione-s-transferase-alpha-3 gene were studied. RESULTS Lipid peroxidation was significantly decreased in ischemic and non-ischemic liver by postconditioning. GST- alpha3 gene was overexpressed in post-conditioned group, but not significantly. CONCLUSION Postconditioning induced hepatoprotection by reducing lipid peroxidation in the ischemic and non-ischemic liver.

[1]  A. Gerbes,et al.  Ischaemic and pharmacological preconditionings protect liver via adenosine and redox status following hepatic ischaemia/reperfusion in rats. , 2008, Clinical science.

[2]  Meijing Wang,et al.  Preconditioning versus postconditioning: mechanisms and therapeutic potentials. , 2006, Journal of the American College of Surgeons.

[3]  J. Downey,et al.  Postconditioning protects rabbit hearts through a protein kinase C-adenosine A2b receptor cascade. , 2006, Cardiovascular research.

[4]  A. Seifalian,et al.  The contemporary role of antioxidant therapy in attenuating liver ischemia‐reperfusion injury: A review , 2005, Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society.

[5]  R. Guyton,et al.  Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine. , 2005, Cardiovascular research.

[6]  E. Botsoglou,et al.  The Protective Effect of α-Tocopherol and GdCl3 Against Hepatic Ischemia/Reperfusion Injury , 2005, Surgery Today.

[7]  Kai Sun,et al.  Role of mitochondria in cell apoptosis during hepatic ischemia-reperfusion injury and protective effect of ischemic postconditioning. , 2004, World journal of gastroenterology.

[8]  J. Downey,et al.  Postconditioning’s protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3–kinase and guanylyl cyclase activation , 2004, Basic Research in Cardiology.

[9]  R. Guyton,et al.  Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. , 2003, American journal of physiology. Heart and circulatory physiology.

[10]  L. Marnett.  Lipid peroxidation-DNA damage by malondialdehyde. , 1999, Mutation research.

[11]  T. Minor,et al.  Involvement of platelet activating factor in microcirculatory disturbances after global hepatic ischemia. , 1995, The Journal of surgical research.

[12]  T. Boyer.  Special article the glutathione S‐transferases: An update , 1989 .

[13]  G. Buckberg,et al.  Reperfusion conditions: importance of ensuring gentle versus sudden reperfusion during relief of coronary occlusion. , 1986, The Journal of thoracic and cardiovascular surgery.