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Başlık: Neuroprotective effects of postconditioning on lipid peroxidation and apoptosis after focal cerebral ischemia/reperfusion injury in rats
Yazarlar: Uludağ Üniversitesi/Tıp Fakültesi/Beyin ve Sinir Cerrahisi Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Patoloji Anabilim Dalı.
0000-0002-2593-7196
Abaş, Faruk
Alkan, Tülin
Gören, Bülent
Taşkapılıoğlu, Özgür
Sarandöl, Emre
Tolunay, Şahsine
ABE-1716-2020
AAH-1718-2021
ABB-8161-2020
AAH-1792-2021
8546184300
6601953747
6602543716
6506852772
55943324800
6602604390
Anahtar kelimeler: Antioxidant enzymes
Ischemia reperfusion injury
Lipid peroxidation
Neuroprotection
Postconditioning
Reduces infarct size
Artery occlusion
Cytochrome-c
Brain-injury
Reperfusion
Ischemia
Protects
Stroke
Mitochondria
Transition
Neurosciences & neurology
Surgery
Yayın Tarihi: Oca-2010
Yayıncı: Türkiye Nöroşirürji Derneği
Atıf: Abaş, F. vd. (2010). "Neuroprotective effects of postconditioning on lipid peroxidation and apoptosis after focal cerebral ischemia/reperfusion injury in rats". Turkish Neurosurgery, 20(1), 1-8.
Özet: 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.
URI: http://turkishneurosurgery.org.tr/pdf/pdf_JTN_712.pdf
http://turkishneurosurgery.org.tr/abstract.php?id=712
http://hdl.handle.net/11452/22654
ISSN: 1019-5149
Koleksiyonlarda Görünür:Scopus
Web of Science

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