Deneysel künt kafa travmasında N-asetilsisteinin sekonder beyin hasarı üzerine etkisi / The effect of N-acetylcysteine on secondary damage in experimental closed head injury
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Tarih
2006
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info:eu-repo/semantics/openAccess
Özet
ÖZET N-asetilsistein' in, glutatyon prekürsörü, antioksidan ve serebest radikal temizleyicisi olarak yararlı etkileri, santral sinir sistemi iskemi ve iskemi/reperfüzyon modelleriyle ortaya konmuştur. Ancak N-asetilsistein'in santral sinir sistemi travmasındaki etkileri daha az anlaşılmıştır. Bu çalışmada, ratlarda oluşturulan deneysel künt kafa travması modeliyle N- asetilsistein'in sekonder hasar üzerine tedavi edici etkisi incelenmeye çalışılmıştır. Otuz altı erkek Sprague-Dawley rat, her bir grupta 12 rat olacak şekilde rastgele üç gruba ayrıldı: Grup 1 (kontrol), Grup 2 (travma), ve Grup 3 (travma + N-asetilsistein tedavisi). Grup 2 ve 3' de, koronal sütürün hemen önünde ve sağ hemisferde bir noktaya gelecek şekilde kafatasına 7 cm yükseklikten bir travma uygulandı. Ratlar, travmadan sonra 2. saatte (Altgrup 1A, 2A ve 3A) ve 12. saatte (Altgrup 1B, 2B ve 3B) sakrifiye edildi. Beyin dokusu biyokimyasal ve histopatolojik inceleme için çıkarıldı. Künt kafa travması kontrollerle kıyaslandığında doku malonildialdehid düzeylerini önemli oranda yükseltti (p< 0.05).Travmadan sonra tek doz N-asetilsistein (150 mg/kg) uygulanması, atmış malonildialdehid düzeylerini önemli oranda düşürerek koruyucu etki gösterdi (p<0.05). Histopatolojik çalışma sonuçları sadece travmaya maruz kalan grupta, nöronların ileri derecede koyulaştığını ve piknotik nukleusta dejenerasyon geliştiğini gösterdi. N-asetilsistein ile tedavi edilen grupta nöronların morfolojisi oldukça iyi korundu. Sadece travmaya maruz kalan grupta nöron sayısı, hem kontrol grubundan hem de travma ile birlikte N-asetilsistein tedavisi uygulanan gruptan ciddi derecede daha düşük bulundu. Sonuçlar, N-asetilsistein tedavisinin travmaya bağlı oksidatif beyin dokusu hasarından korunma için faydalı olabileceğini ortaya koydu. Anahtar sözcükler: Beyin dokusu, malonildialdehid , caspase-3, kafa travması, rat, N-asetilsistein
THE EFFECT OF N-ACETYLCYSTEINE ON SECONDARY DAMAGE IN EXPERIMENTAL CLOSED HEAD INJURY SUMMARY The beneficial effect of N-acetylcysteine as a precursor of glutathione, an antioxidant, and a free radical scavenger on nervous system ischemia and ischemia/reperfusion models has been well documented. However, the effect of N-acetylcysteine on nervous system trauma remains less understood. In this study, we aimed to investigate the therapeutic efficacy of N- acetylcysteine with an experimental closed head trauma model in rats. Thirty-six adult male Sprague-Dawley rats were randomly divided into three groups of 12 rats each: Group 1 (control), Group 2 (trauma-alone), and Group 3 (trauma+ N- acetylcysteine treatment). In Groups 2 and 3, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 2 h (Subgroups 1A, 2A, and 3A) and 12 h (Subgroups 1B, 2B, and 3B) after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. The closed head trauma significantly increased tissue malondialdehyde levels (p< 0.05) when compared with controls. The administration of a single dose of N- acetylcysteine (150 mg/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated malondialdehyde levels (p < 0.05). The histopathological study revealed that in the trauma-alone group, the neurons became extensively dark and degenerated into picnotic nuclei. The morphology of neurons in the N-acetylcysteine treatment group was well protected. The number of neurons in the trauma-alone group was significantly less than that of both the control and trauma+ N- acetylcysteine treatment groups. In conclusion, the N-acetylcysteine treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage. Key words: Brain tissue, malondialdehyde, caspase-3, head injury, rat, N- acetylcysteine
THE EFFECT OF N-ACETYLCYSTEINE ON SECONDARY DAMAGE IN EXPERIMENTAL CLOSED HEAD INJURY SUMMARY The beneficial effect of N-acetylcysteine as a precursor of glutathione, an antioxidant, and a free radical scavenger on nervous system ischemia and ischemia/reperfusion models has been well documented. However, the effect of N-acetylcysteine on nervous system trauma remains less understood. In this study, we aimed to investigate the therapeutic efficacy of N- acetylcysteine with an experimental closed head trauma model in rats. Thirty-six adult male Sprague-Dawley rats were randomly divided into three groups of 12 rats each: Group 1 (control), Group 2 (trauma-alone), and Group 3 (trauma+ N- acetylcysteine treatment). In Groups 2 and 3, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 2 h (Subgroups 1A, 2A, and 3A) and 12 h (Subgroups 1B, 2B, and 3B) after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. The closed head trauma significantly increased tissue malondialdehyde levels (p< 0.05) when compared with controls. The administration of a single dose of N- acetylcysteine (150 mg/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated malondialdehyde levels (p < 0.05). The histopathological study revealed that in the trauma-alone group, the neurons became extensively dark and degenerated into picnotic nuclei. The morphology of neurons in the N-acetylcysteine treatment group was well protected. The number of neurons in the trauma-alone group was significantly less than that of both the control and trauma+ N- acetylcysteine treatment groups. In conclusion, the N-acetylcysteine treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage. Key words: Brain tissue, malondialdehyde, caspase-3, head injury, rat, N- acetylcysteine
Açıklama
Anahtar Kelimeler
Nöroşirürji, Neurosurgery
