Thiamine preserves mitochondrial function in a rat model of traumatic brain injury, preventing inactivation of the 2-oxoglutarate dehydrogenase complex

Based on the fact that traumatic brain injury is associated with mitochondrial dysfunction we aimed at localization of mitochondrial defect and attempted to correct it by thiamine. Interventional controlled experimental animal study was used. Adult male Sprague-Dawley rats were subjected to lateral...

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Veröffentlicht in:	Biochimica et biophysica acta. Bioenergetics 2018-09, Vol.1859 (9), p.925-931
Hauptverfasser:	Mkrtchyan, Garik V., Üçal, Muammer, Müllebner, Andrea, Dumitrescu, Sergiu, Kames, Martina, Moldzio, Rudolf, Molcanyi, Marek, Schaefer, Samuel, Weidinger, Adelheid, Schaefer, Ute, Hescheler, Juergen, Duvigneau, Johanna Catharina, Redl, Heinz, Bunik, Victoria I., Kozlov, Andrey V.
Format:	Artikel
Sprache:	eng
Schlagworte:	2-Oxoglutarate dehydrogenase complex Animals Biomarkers - metabolism Brain Injuries, Traumatic - physiopathology Energy Metabolism Gene Expression Regulation - drug effects Ketoglutarate Dehydrogenase Complex - antagonists & inhibitors Ketoglutarate Dehydrogenase Complex - genetics Ketoglutarate Dehydrogenase Complex - metabolism Male Mitochondria Mitochondria - drug effects Mitochondria - physiology Neurogenic Inflammation - etiology Neurogenic Inflammation - metabolism Neurogenic Inflammation - prevention & control Neuroinflammation Nitric Oxide Synthase Type II - metabolism Oxidation-Reduction Rats Rats, Sprague-Dawley Receptors, Tumor Necrosis Factor, Type I - metabolism TCA cycle Thiamine Thiamine - pharmacology Traumatic brain injury (TBI) Vitamin B Complex - pharmacology
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