The beneficial effects of 18 glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia reperfusion in a C57BL J6 mouse model

Basit Öğe Kaydı
dc.authoridTR107942en_US
dc.authoridTR102040en_US
dc.authoridTR52354en_US
dc.authoridTR60444en_US
dc.authoridTR103979en_US
dc.contributor.authorÖztanır, Mustafa Namık
dc.contributor.authorÇiftçi, Osman
dc.contributor.authorÇetin, Aslı
dc.contributor.authorDurak, Mehmet Akif
dc.contributor.authorBaşak, Neşe
dc.contributor.authorAkyuva, Yener
dc.date.accessioned2017-04-17T13:18:30Z
dc.date.available2017-04-17T13:18:30Z
dc.date.issued2014
dc.departmentİnönü Üniversitesien_US
dc.description.abstractThis study investigated the effects of 18bglycyrrhetinic acid (GA) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. All subjects (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) I/R, (3) GA, and (4) GA?I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with the vehicle for 10 days. In the GA group, mice were given GA (100 mg/ kg) for 10 days following a median incision without carotid occlusion. In the GA?I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with the same dose of GA for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidaitons and a decrease in elements of the antioxidant defense systems. However, GA treatment was protective against the oxidative effects of I/R by inducing significant increases in antioxidant defense systems and a significant decrease of lipid peroxidations. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by GA treatment. Therefore, the current study demonstrated that GA treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, GA may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, it may be a viable and safe alternative treatment for ischemic stroke in humans.en_US
dc.identifier.citationÖztanır, M. N. Çiftçi, O. Çetin, A. Durak, M. A. Başak, N. Akyuva, Y. (2014). The beneficial effects of 18 glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia reperfusion in a C57BL J6 mouse model . Neurol Sci, 35:1221–1228.en_US
dc.identifier.doi10.1007/s10072-014-1685-9en_US
dc.identifier.endpage1228en_US
dc.identifier.startpage1221en_US
dc.identifier.urihttps://hdl.handle.net/11616/6681
dc.identifier.volume35en_US
dc.language.isoenen_US
dc.publisherNeurol Scien_US
dc.relation.ispartofNeurol Scien_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectGlobal cerebral I/Ren_US
dc.subjectOxidative stressen_US
dc.subjectNeuronal damageen_US
dc.subjectGlycyrrhetinic aciden_US
dc.subjectC57BL/J6 mice Inen_US
dc.titleThe beneficial effects of 18 glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia reperfusion in a C57BL J6 mouse modelen_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
Küçük Resim
İsim:
Makale Dosyası.pdf
Boyut:
8.84 MB
Biçim:
Adobe Portable Document Format
Açıklama:
Makale Dosyası
İndir
Lisans paketi
Listeleniyor 1 - 1 / 1
Küçük Resim Yok
İsim:
license.txt
Boyut:
1.71 KB
Biçim:
Item-specific license agreed upon to submission
Açıklama:
İndir

Koleksiyon

Sağlık Bilimleri Enstitüsü Diğer Yayınlar Koleksiyonu