Effects of tadalafil on ischemia/reperfusion injury in rat brain
Yükleniyor...
Dosyalar
Tarih
2014
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Springer Heidelberg
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Cerebral ischemia-reperfusion (I/R) injury is caused by lack of blood supply to the brain. The accumulation of toxic products such as reactive oxygen species (ROS) occurs on reperfusion, when the occlusion is removed. The resulting oxidative stress results in the initiation of pathways leading to necrotic and apoptotic cell death. Tadalafil (TAD) prevents the accumulation of ROS and increases antioxidant cellular protective mechanisms. The aim of this study was to investigate the effect of TAD treatment against short-term global brain I/R injury in rats. The study was carried out on 30 Wistar-albino rats, which were divided into three groups including a control group (n = 10), an I/R group (n = 10) and an I/R + TAD group (n = 10) (2 mg/kg/day for 4 days before ischemia). At the end of the experiment, tissue samples were collected for both biochemical and histopathological analyses. Malondialdehyde was significantly lower in the TAD-administered group (9.06 +/- A 0.15) than in the I/R group (p < 0.05). However, no significant difference was observed in nitric oxide levels in the TAD-administered group compared to the I/R group. The mean superoxide dismutase level was significantly higher in the I/R-TAD group than the I/R group. There was no statistically significant difference in glutathione peroxidase levels in I/R + TAD group compared to I/R group. Histopathologically, TAD-administered group provided significant morphological improvement compared to the I/R group. We concluded that TAD prevented I/R-induced neurotoxicity as shown by obtained biochemical and histopathological findings.
Açıklama
Anahtar Kelimeler
Tadalafil, Brain, Ischemia/reperfusion
Kaynak
Acta Neurologica Belgica
WoS Q Değeri
Q4
Scopus Q Değeri
Q2
Cilt
114
Sayı
1
