Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury
المؤلفون المشاركون
Kupats, Einars
Stelfa, Gundega
Zvejniece, Baiba
Grinberga, Solveiga
Vavers, Edijs
Makrecka-Kuka, Marina
Svalbe, Baiba
Zvejniece, Liga
Dambrova, Maija
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-11-21
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص EN
Altered neuronal Ca2+ homeostasis and mitochondrial dysfunction play a central role in the pathogenesis of traumatic brain injury (TBI).
R-Phenibut ((3R)-phenyl-4-aminobutyric acid) is an antagonist of the α2δ subunit of voltage-dependent calcium channels (VDCC) and an agonist of gamma-aminobutyric acid B (GABA-B) receptors.
The aim of this study was to evaluate the potential therapeutic effects of R-phenibut following the lateral fluid percussion injury (latFPI) model of TBI in mice and the impact of R- and S-phenibut on mitochondrial functionality in vitro.
By determining the bioavailability of R-phenibut in the mouse brain tissue and plasma, we found that R-phenibut (50 mg/kg) reached the brain tissue 15 min after intraperitoneal (i.p.) and peroral (p.o.) injections.
The maximal concentration of R-phenibut in the brain tissues was 0.6 μg/g and 0.2 μg/g tissue after i.p.
and p.o.
administration, respectively.
Male Swiss-Webster mice received i.p.
injections of R-phenibut at doses of 10 or 50 mg/kg 2 h after TBI and then once daily for 7 days.
R-Phenibut treatment at the dose of 50 mg/kg significantly ameliorated functional deficits after TBI on postinjury days 1, 4, and 7.
Seven days after TBI, the number of Nissl-stained dark neurons (N-DNs) and interleukin-1beta (IL-1β) expression in the cerebral neocortex in the area of cortical impact were reduced.
Moreover, the addition of R- and S-phenibut at a concentration of 0.5 μg/ml inhibited calcium-induced mitochondrial swelling in the brain homogenate and prevented anoxia-reoxygenation-induced increases in mitochondrial H2O2 production and the H2O2/O ratio.
Taken together, these results suggest that R-phenibut could serve as a neuroprotective agent and promising drug candidate for treating TBI.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Kupats, Einars& Stelfa, Gundega& Zvejniece, Baiba& Grinberga, Solveiga& Vavers, Edijs& Makrecka-Kuka, Marina…[et al.]. 2020. Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1206031
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Kupats, Einars…[et al.]. Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1206031
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Kupats, Einars& Stelfa, Gundega& Zvejniece, Baiba& Grinberga, Solveiga& Vavers, Edijs& Makrecka-Kuka, Marina…[et al.]. Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1206031
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1206031
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر