Neuroprotective Effects of Postconditioning on Lipid Peroxidation and Apoptosis after Focal Cerebral Ischemia/Reperfusion Injury in Rats

AIM: Apoptosis after cerebral ischemia/reperfusion (I/R) injury leads to the process of cell death. The deal therapeutic approach would target the apoptosis after I/R. Ischemic postconditioning is a recently discovered neuroprotective strategy that involves the application of brief mechanical reperfusion with a specific algorithm at the onset of reperfusion following an ischemic period. MATERIAL and METHODS: Transient MCAo was performed on male SD (275 +/- 25g) rats with intraluminal thread insertion for 2hrs. Rats (n:36) were treated with postconditioning after 60 minutes of occlusion. The postconditioning algorithm was 30 secs of brief reperfusion followed by 30 secs of MCAo and this cycle was repeated 3 times at the onset of reperfusion. RESULTS: After I/R injury, % change of the malonyldialdehyde (MDA) levels in the cortex, which is an index of lipid peroxidation, was found significantly higher in the I/R group. On the other hand postconditioning upregulated Bcl-2 and Bax translocation to the mitochondria, and caspase-3 activity and also reduced oxidative stress levels. CONCLUSION: These findings indicated this neuroprotective effect is most likely achieved by antiapoptotic mechanisms through caspase pathways. KEYWORDS: Antioxidant enzymes, Ischemia reperfusion injury, Lipid peroxidation, Neuroprotection, Postconditioning