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+/-25 g) rats with intraluminal thread insertion for 2 hrs. 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.
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+/-25 g) rats with intraluminal thread insertion for 2 hrs. 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.
Authors: Tarık Akman; Mustafa Guven; Adem Bozkurt Aras; Adile Ozkan; Halil Murat Sen; Ali Okuyucu; Yildiray Kalkan; Ibrahim Sehitoglu; Coskun Silan; Murat Cosar Journal: Inflammation Date: 2015-08 Impact factor: 4.092
Authors: Xue Fei Han; Yuan Zhang; Liu Lin Xiong; Yang Xu; Piao Zhang; Qing Jie Xia; Ting Hua Wang; Ying Chun Ba Journal: Mol Neurobiol Date: 2016-02-12 Impact factor: 5.590