The effects of selenium against cerebral ischemia-reperfusion injury in rats.
It is known that the brain tissue is extremely sensitive to ischemia-reperfusion (IR) injury and therefore, brain ischemia and consecutive reperfusion result in neural damage and apoptosis. The proinflammatory cytokines such as tumor necrosis factor alfa (TNF-alpha) and interleukin-1 beta (IL-1beta) are produced during neurological disorders including cerebral ischemia. On the other hand, nerve growth factor (NGF), which is essential for the differentiation, survival and functions of neuronal cells in the central nervous system, regulate neuronal development through cell survival and cell death signaling. In the present study, we aimed to investigate the effect of selenium (Se) on prefrontal cortex and hippocampal damage in rats subjected to cerebral IR injury. Selenium was injected intraperitoneally at the doses of 0.625 mg/(kg day) after induction of IR injury. Prefrontal cortex and hippocampal damage was examined by cresyl-violet staining. Apostain and caspase-3 immune staining were used to detect apoptosis. TNF-alpha, IL-1beta and NGF levels were also evaluated. Histopathological evaluation showed that treatment with selenium after ischemia significantly attenuated IR-induced neuronal death in prefrontal cortex and hippocampal CA1 regions of rats. Apoptotic cells stained with apostain and caspase-3 were significantly decreased in treatment group when compared with the IR group. Additionally, treatment with selenium decreased the TNF-alpha and IL-1beta levels and increased the NGF levels in prefrontal cortex and hippocampal tissue of animals subjected to IR. The present results suggest that selenium is potentially a beneficial agent in treating IR-induced brain injury in rats.
Ozbal
Seda
S
Department of Histology and Embryology, School of Medicine, Dokuz Eylul University Inciralti, TR-35340, Izmir, Turkey. seda.ozbal@deu.edu.tr
Erbil
Güven
G
Koçdor
Hilal
H
Tuğyan
Kazim
K
Pekçetin
Cetin
C
Ozoğul
Candan
C
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D006624:Hippocampus / Q000187:drug effects; D020287:In Situ Nick-End Labeling; D053583:Interleukin-1beta; D008297:Male; D009414:Nerve Growth Factors; D017397:Prefrontal Cortex / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000473:pathology*; D012643:Selenium / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha
D000975:Antioxidants; D053583:Interleukin-1beta; D009414:Nerve Growth Factors; D014409:Tumor Necrosis Factor-alpha; D053148:Caspase 3; D012643:Selenium