Deneysel kafa travması modelinde dekspantenolün nöroprotektif etkililiğinin araştırılması
Küçük Resim Yok
Tarih
2022
Yazarlar
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Cilt Başlığı
Yayıncı
İnönü Üniversitesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Deneysel Kafa Travması Modelinde Dekspantenol'ün Nöroprotektif Etkililiğinin Araştırılması Amaç: Travmatik beyin hasarı sonrasında gelişen inflamasyon, apopitoz ve oksidatif stres beyin dokusundaki hasarın şiddetlenmesine yol açmaktadır. Nöroprotektif etkileri bilinen dekspantenolün çeşitli deneysel modellerde ve iskemik hastalıklarda yararlı olduğu gösterilmiştir. Bu çalışmada travmatik beyin hasarı modelinde dekspantenolün (DXP) olası antiinflamatuar, antiapopitotik, antioksidan ve nöroprotektif etkilerinin incelenmesi amaçlanmıştır. Materyal ve Metod: Araştırmada yaklaşık 6 aylık, 220-285 gr. ağırlığında 36 adet Wistar-Albino cinsi dişi rat kullanıldı. Bütün ratlar, hazırlanan kafa travması modeli düzeneğinde parietal bölge üzerine 50cm yükseklikten180 derece açıyla, 350 gr. ağırlık düşürülerek, kapalı kafa travması oluşturuldu. Ratlar kontrol grubunda (Grup-1) 8,travma grubunda (Grup-2) 10, travma+ DXP grubunda (Grup-3) 10 ve DXP grubunda( Grup-4) 8adet olacak şekilde 4 grupta incelendi. Kontrol grubunda kafa travması oluştuulmadı ve DPX uygulanmadı.Grup-2 de kafa travması oluşturuldu fakat DXP uygulanmadı. Grup-3'te kafa travmasıoluşturulan ratlara30.dakika, 6. saat, 12. saat, 24 saat, 36. saat ve 48. saatlerinde toplam 6 kez DXP 500 mg/kg dozunda intraperitoneal(ip) olarak uygulandı. 4.gruba kafa travması oluşturulmadan Grup-3 ile eş zamanlı olarak DXP intraperitoneal (ip) verilerek çalışma yapıldı. Tüm ratlardan 72 saat sonra biyokimyasal inceleme için kan örnekleri alındı. Kan örnekleri alındıktan sonra ratlar genel anestezi altında dekapite edildi. Dekapite edilen ratlardan immünohistokimyasal ve histopatolojik inceleme için serebral doku örnekleri alındı. Bulgular: Travma sonrası beyin dokusunda değerlendirilen sitokin markerlarında artış bulundu.Malondialdehit ve glutatyon redüktaz düzeylerinin travma sonrası DXP verilen grupta travma grubuna göre daha düşük olduğu bulundu (p<0.05). Ayrıca süperoksid dismutaz,glutatyon peroksidaz ve katalaz düzeylerinin travma sonrası DXP verilen grupta travma grubuna göre daha anlamlı olarak daha yüksek olduğu saptandı.(p<0.05) Histolojik değerlendirmede travma sonrası DXP verilen Grup-sadece travma grubuna kıyaslandığındabeyin dokusunda piamater tabakasında konjesyon, hücre infiltrasyonu, vasküler konjesyon, hemoraji ve nöron dejenerasyonun belirgin derecede azalma gösterdiği belirlendi. Sonuç: Sıçanlarda kafa travması sonrasıDXP'nin histolojik ve oksidatif değişiklikler açısından nörolojik iyileşmede faydalı olduğugörülmektedir.Grup-4'teki sıçanların beyin dokularına oksidatif hasar ve apoptoz baskılandığı sonucuna ulaşıldı. DXP'nin travmatik beyin hasarındaki olası terapötik etkisi açısından daha fazla değerlendirilmesi gerekmektedir.
Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model Aim: Inflammation, apoptosis and oxidative stress that develop after traumatic brain injury lead to further aggravation of damage to brain tissue. Dexpanthenol, whose neuroprotective effects are known, has been shown to be useful in various experimental models and ischemic diseases. In this study, the traumatic it is aimed to investigate the possible anti-inflammatory, antiapoptotic, antioxidant and neuroprotective effects of dexpanthenol (DXP)in a brain injury model. Material and Method: In this study, 36 Wistar-Albino female rats weighing approximately 6 months old and weighing 220-285 gr. were used. All rats were injured by reducing the weight of 350 g at an angle of 180 degrees from a height of 50 cm to the parietal region in the prepared head injury model mechanism. Rats were examined in 4 groups, 8 in the control group (Group 1), 10 in the trauma group (Group 2), 10 in the trauma+ DXP group (Group 3) and 8 in the DXP group (Group 4). In group 1, no head injury was created, DXP was not given, in group 2, a head injury was created, but DXP was not given. 30 After a head injury in Group 3.minutes, 6. it's 12 o'clock. hour, 24 hours, 36. hours and 48. DXP was administered intraperitoneally(ip) at a dose of 500 mg/kg a total of 6 times per hour. 4.the study was performed by administering DXP intraperitoneal (ip) simultaneously with group 3 without causing head trauma to the group. after 72 hours, blood samples were taken from all rats for biochemical examination, and then all rats were decapitated under general anesthesia and cerebral tissue samples were taken for immunohistochemical and histopathological examination. Results: All cytokines were increased in the post-traumatic brain tissue. Compared to the trauma group, the post-traumatic dexpanthenol group had lower malondialdehyde and glutathione reductase levels; The levels of superoxide dismutase, glutathione peroxidase and catalase were found to be significantly higher. (p<0.05) Histologically, a significant decrease was observed in the piamater layer of the brain tissue, such as congestion, cell infiltration, vascular congestion, hemorrhage and neuron degeneration in the posttraumatic dexpanthenol group compared to the trauma group. Conclusion: , We found that after head trauma in rats, DXP were beneficial in neurologic recovery on histologically and with respect to oxidative changes.The brain tissues of rats in the DXP group was suppressioned of oxidative damage and apoptosis. We suggest that DXP should be further evaluated for its possible therapeutic effect in traumatic brain injury.
Investigation of Neuroprotective Efficacy of Dexpanthenol in an Experimental Head Injury Model Aim: Inflammation, apoptosis and oxidative stress that develop after traumatic brain injury lead to further aggravation of damage to brain tissue. Dexpanthenol, whose neuroprotective effects are known, has been shown to be useful in various experimental models and ischemic diseases. In this study, the traumatic it is aimed to investigate the possible anti-inflammatory, antiapoptotic, antioxidant and neuroprotective effects of dexpanthenol (DXP)in a brain injury model. Material and Method: In this study, 36 Wistar-Albino female rats weighing approximately 6 months old and weighing 220-285 gr. were used. All rats were injured by reducing the weight of 350 g at an angle of 180 degrees from a height of 50 cm to the parietal region in the prepared head injury model mechanism. Rats were examined in 4 groups, 8 in the control group (Group 1), 10 in the trauma group (Group 2), 10 in the trauma+ DXP group (Group 3) and 8 in the DXP group (Group 4). In group 1, no head injury was created, DXP was not given, in group 2, a head injury was created, but DXP was not given. 30 After a head injury in Group 3.minutes, 6. it's 12 o'clock. hour, 24 hours, 36. hours and 48. DXP was administered intraperitoneally(ip) at a dose of 500 mg/kg a total of 6 times per hour. 4.the study was performed by administering DXP intraperitoneal (ip) simultaneously with group 3 without causing head trauma to the group. after 72 hours, blood samples were taken from all rats for biochemical examination, and then all rats were decapitated under general anesthesia and cerebral tissue samples were taken for immunohistochemical and histopathological examination. Results: All cytokines were increased in the post-traumatic brain tissue. Compared to the trauma group, the post-traumatic dexpanthenol group had lower malondialdehyde and glutathione reductase levels; The levels of superoxide dismutase, glutathione peroxidase and catalase were found to be significantly higher. (p<0.05) Histologically, a significant decrease was observed in the piamater layer of the brain tissue, such as congestion, cell infiltration, vascular congestion, hemorrhage and neuron degeneration in the posttraumatic dexpanthenol group compared to the trauma group. Conclusion: , We found that after head trauma in rats, DXP were beneficial in neurologic recovery on histologically and with respect to oxidative changes.The brain tissues of rats in the DXP group was suppressioned of oxidative damage and apoptosis. We suggest that DXP should be further evaluated for its possible therapeutic effect in traumatic brain injury.
Açıklama
Anahtar Kelimeler
Nöroşirürji, Neurosurgery
