The effect of allopurinol and acetylsalicylate on ischemia-reperfusion related injury of liver
Küçük Resim Yok
Tarih
1999
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Dokularda iskemi sırasında meydana gelen hasarın reperfüzyon sırasında arttığı, bu artışın da biyomembranlarda oksijen kaynaklı serbest radikallerin yol açtığı lipid peroksidasyonundan kaynaklandığı kabul edilir. Serbest radikaller çeşitli kaynaklardan oluşurlar. Bu kaynaklardan ikisi; ksantin oksidaz sistemi ve araşidonik asit yoludur. Bu çalışmanın amacı, bu sistemlerin lipid peroksidasyonu ve serbest oksijen radikalleri üretimi üzerine olan etkisini karaciğer iskemi-reperfüzyonu rat modeliyle değerlendirmektir. Bu maksat için 28 Wistar albino rat 5 gruba ayrıldı. Kontrol grubundaki ratlar üzerinde operasyon yapılmadı. İkinci grupta hepatik arterin sağ üst kolu ve portal ven 90 dakika süre ile klempe edilmek suretiyle iskemi oluşturuldu. Üçüncü grupta 90 dakikalık iskemi periyodu sonunda klampları açmak suretiyle 30 dakika süre ile reperfüzyon sağlandı. Aynı iskemi ve reperfüzyon işlemleri, allopurinol verilen dördüncü grup ve asetilsalisilat verilen beşinci grup ratlar üzerine uygulandı. Allopurinol ve asetilsalisilat oral yoldan işlemlerden önce üç gün süre ile verildi. Bütün gruplarda tiobarbitürat metodu kullanarak malondialdehit-tiobarbiturik asid (MDA-TBA) seviyelerini ölçmek suretiyle lipid peroksidasyonu değerlendirildi. İskeminin lipid peroksidasyonunu arttırdığı, bu artışın reperfüzyon sırasında fazlalaştığı görüldü. Lipid peroksidasyonu reperfüzyon grubu ile karşılaştırıldığında allopurinol grubunda anlamlı bir şekilde azaldığı (p0.001) görülürken asetilsalisilat grubunda değişmediği gözlendi. Bulgularımız, iskemi-reperfüzyon ile ilgili karaciğer hasarı üzerinde ksantin oksidaz sisteminin araşidonik asit yolundan daha etkili olduğunu, allopurinolün iskemi-reperfüzyon hasarı üzerine koruyucu bir etkiye sahip olduğunu göstermektedir.
It is assumed that, the injury which occurs in tissues during ischemia period increases during reperfusion period, and this increase is due to lipid peroxidation caused by oxygen derived free radicals in biomembranes. Free radicals are formed through various mechanisms and two of them are xanthine oxidase system and arachidonic acid pathway. The aim of the present study is to evaluate the effect of these systems on free oxygen radicals production and lipid peroxidation by using allo-purinol (a xanthine oxidase inhibitor) and acetylsalicylate (an inhibitor of arachidonic acid metabolism) in the rat model of liver ischemia - reperfusion. For that purpose, 28 Wistar albino rats were divided into five groups. No operation was performed on the rats in the control group. Ischemia was induced by clamping right upper branches of hepatic artery and portal vein for 90 minutes in the second group. In the third group, after 90 minutes of ischemia period, reperfusion was achieved by opening the clamps for 30 minutes. The same ischemia and reperfusion procedures were performed on the allopurinol pretreated rats in the fourth group and on the acetylsalicylate pretreated rats in the fifth group. Allopurinol and acetylsalicylate were administered by oral route for three days before the procedures. In all groups, lipid peroxidation was evaluated by measuring malondialdehyde-thiobarbituric acid (MDA-TBA) levels using thiobarbiturate method. It was observed that ischemia increased lipid peroxidation and this increase was enhanced during reperfusion period. In the allopurinol group, lipid peroxidation significantly diminished compared with reperfusion group (p<0.001) while no change was observed in the acetylsalicylate group. Our findings suggest that xanthine oxidase system is more effective than arachidonic acid pathway on ischemia-reperfusion related injury of liver and, allopurinol has a protective effect on ischemia - reperfusion injury
It is assumed that, the injury which occurs in tissues during ischemia period increases during reperfusion period, and this increase is due to lipid peroxidation caused by oxygen derived free radicals in biomembranes. Free radicals are formed through various mechanisms and two of them are xanthine oxidase system and arachidonic acid pathway. The aim of the present study is to evaluate the effect of these systems on free oxygen radicals production and lipid peroxidation by using allo-purinol (a xanthine oxidase inhibitor) and acetylsalicylate (an inhibitor of arachidonic acid metabolism) in the rat model of liver ischemia - reperfusion. For that purpose, 28 Wistar albino rats were divided into five groups. No operation was performed on the rats in the control group. Ischemia was induced by clamping right upper branches of hepatic artery and portal vein for 90 minutes in the second group. In the third group, after 90 minutes of ischemia period, reperfusion was achieved by opening the clamps for 30 minutes. The same ischemia and reperfusion procedures were performed on the allopurinol pretreated rats in the fourth group and on the acetylsalicylate pretreated rats in the fifth group. Allopurinol and acetylsalicylate were administered by oral route for three days before the procedures. In all groups, lipid peroxidation was evaluated by measuring malondialdehyde-thiobarbituric acid (MDA-TBA) levels using thiobarbiturate method. It was observed that ischemia increased lipid peroxidation and this increase was enhanced during reperfusion period. In the allopurinol group, lipid peroxidation significantly diminished compared with reperfusion group (p<0.001) while no change was observed in the acetylsalicylate group. Our findings suggest that xanthine oxidase system is more effective than arachidonic acid pathway on ischemia-reperfusion related injury of liver and, allopurinol has a protective effect on ischemia - reperfusion injury
Açıklama
Anahtar Kelimeler
Genel ve Dahili Tıp
Kaynak
Türkiye Klinikleri Tıp Bilimleri Dergisi
WoS Q Değeri
Scopus Q Değeri
Cilt
19
Sayı
2
