Effect of Coenzyme Q(10) on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats

Background: Head trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q(10) (CoQ(10)), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ(10) in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ(10) administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out. Results: In the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (p < 0.05). Administration of CoQ(10) after trauma was shown to be protective because it significantly lowered the increased MDA levels (p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ(10) group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ(10) and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p < 0.05). Conclusion: Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ(10) use in rats with traumatic brain injury.

Yazar Kalayci, Murat
Unal, Mufit M.
Gul, Sanser
Acikgoz, Serefden
Kandemir, Nilufer
Hanci, Volkan
Edebali, Nurullah
Yayın Türü Article
Tek Biçim Adres https://hdl.handle.net/20.500.12628/2440
Tek Biçim Adres 10.1186/1471-2202-12-75
Koleksiyonlar Araştırma Çıktıları | WoS | Scopus | TR-Dizin | PubMed | SOBİAD
PubMed İndeksli Yayınlar Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu
Dergi Adı BMC NEUROSCIENCE
Dergi Cilt Bilgisi 12
Sayfalar -
Yayın Yılı 2011
Eser Adı
[dc.title]
Effect of Coenzyme Q(10) on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats
Yazar
[dc.contributor.author]
Kalayci, Murat
Yazar
[dc.contributor.author]
Unal, Mufit M.
Yazar
[dc.contributor.author]
Gul, Sanser
Yazar
[dc.contributor.author]
Acikgoz, Serefden
Yazar
[dc.contributor.author]
Kandemir, Nilufer
Yazar
[dc.contributor.author]
Hanci, Volkan
Yazar
[dc.contributor.author]
Edebali, Nurullah
Yayın Yılı
[dc.date.issued]
2011
Yayıncı
[dc.publisher]
BIOMED CENTRAL LTD
Yayın Türü
[dc.type]
article
Özet
[dc.description.abstract]
Background: Head trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q(10) (CoQ(10)), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ(10) in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ(10) administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out. Results: In the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (p < 0.05). Administration of CoQ(10) after trauma was shown to be protective because it significantly lowered the increased MDA levels (p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ(10) group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ(10) and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p < 0.05). Conclusion: Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ(10) use in rats with traumatic brain injury.
Açıklama
[dc.description]
WOS: 000294217100001
Açıklama
[dc.description]
PubMed: 21801363
Kayıt Giriş Tarihi
[dc.date.accessioned]
2019-12-23
Açık Erişim Tarihi
[dc.date.available]
2019-12-23
Yayın Dili
[dc.language.iso]
eng
Haklar
[dc.rights]
info:eu-repo/semantics/openAccess
ISSN
[dc.identifier.issn]
1471-2202
Dergi Adı
[dc.relation.journal]
BMC NEUROSCIENCE
Dergi Cilt Bilgisi
[dc.identifier.volume]
12
Tek Biçim Adres
[dc.identifier.uri]
https://dx.doi.org/10.1186/1471-2202-12-75
Tek Biçim Adres
[dc.identifier.uri]
https://hdl.handle.net/20.500.12628/2440
Görüntülenme Sayısı ( Şehir )
Görüntülenme Sayısı ( Ülke )
Görüntülenme Sayısı ( Zaman Dağılımı )
Görüntülenme
7
09.12.2022 tarihinden bu yana
İndirme
1
09.12.2022 tarihinden bu yana
Son Erişim Tarihi
27 Ocak 2024 19:29
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Tıklayınız
CoQ(10) trauma traumatic levels between brain-injury damage statistically secondary ischemia neuronal significantly groups midline biochemical significant injury treatment decreased nuclear Histopathological degenerative compared findings Conclusion Neuronal higher axonal eosinophilia caused oxidative stress Administration malondialdehyde tissue
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