Turkish Neurosurgery 2010 , Vol 20 , Num 1
Neuroprotective Effects of Postconditioning on Lipid Peroxidation and Apoptosis after Focal Cerebral Ischemia/Reperfusion Injury in Rats
Faruk ABAS1, Tulin ALKAN2, Bulent GOREN3, Ozgur TASKAPILIOGLU4, Emre SARANDOL5, Sahsene TOLUNAY6
1,3,4Uludag University, Faculty of Medicine, Department of Neurosurgery, Bursa, Turkey
2Uludag University, Faculty of Medicine, Department of Physiology, Bursa, Turkey
5Uludag University, Faculty of Medicine, Department of Biochemistry, Bursa, Turkey
6Uludag University, Faculty of Medicine, Department of Pathology, Bursa, Turkey
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

Corresponding author : Tulin Alkan, talkan@uludag.edu.tr