Kupats 2020 Oxid Med Cell Longev: Difference between revisions
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{{Publication | {{Publication | ||
|title=Kupats E, Stelfa G,Zvejniece B, Grinberga S,Vavers E, Makrecka-Kuka M, Svalbe B, Zvejniece L, Dambrova M (2020) Mitochondrial-protective effects of R-phenibut after experimental traumatic brain injury. Oxid Med Cell Longev 2020:9364598 . | |title=Kupats E, Stelfa G, Zvejniece B, Grinberga S, Vavers E, Makrecka-Kuka M, Svalbe B, Zvejniece L, Dambrova M (2020) Mitochondrial-protective effects of R-phenibut after experimental traumatic brain injury. Oxid Med Cell Longev 2020:9364598. | ||
|info=[https://www.hindawi.com/journals/omcl/2020/9364598/ Open Access] | |info=[https://www.hindawi.com/journals/omcl/2020/9364598/ Open Access] | ||
|authors=Kupats | |authors=Kupats Einars, Stelfa Gundega, Zvejniece Baiba, Grinberga Solveiga, Vavers Edijs, Makrecka-Kuka Marina, Svalbe Baiba, Zvejniece Liga, Dambrova Maija | ||
|year=2020 | |year=2020 | ||
|journal=Oxid Med Cell Longev | |journal=Oxid Med Cell Longev | ||
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{{Labeling | {{Labeling | ||
|area=Respiration, Pharmacology;toxicology | |area=Respiration, Pharmacology;toxicology | ||
|instruments=Oxygraph-2k | |diseases=Other | ||
|additional=2020-11 | |organism=Mouse | ||
|tissues=Nervous system | |||
|preparations=Homogenate, Isolated mitochondria | |||
|couplingstates=LEAK, OXPHOS, ET | |||
|pathways=N, S, NS | |||
|instruments=Oxygraph-2k, O2k-Fluorometer | |||
|additional=2020-11, AmR | |||
}} | }} |
Latest revision as of 17:16, 26 November 2020
Kupats E, Stelfa G, Zvejniece B, Grinberga S, Vavers E, Makrecka-Kuka M, Svalbe B, Zvejniece L, Dambrova M (2020) Mitochondrial-protective effects of R-phenibut after experimental traumatic brain injury. Oxid Med Cell Longev 2020:9364598. |
Β» Open Access
Kupats Einars, Stelfa Gundega, Zvejniece Baiba, Grinberga Solveiga, Vavers Edijs, Makrecka-Kuka Marina, Svalbe Baiba, Zvejniece Liga, Dambrova Maija (2020) Oxid Med Cell Longev
Abstract: 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 Ξ±2Ξ΄ 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 (50βmg/kg) reached the brain tissue 15βmin after intraperitoneal (i.p.) and peroral (p.o.) injections. The maximal concentration of R-phenibut in the brain tissues was 0.6βΞΌg/g and 0.2βΞΌg/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 50βmg/kg 2βh after TBI and then once daily for 7 days. R-Phenibut treatment at the dose of 50βmg/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-1Ξ²) 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 0.5βΞΌg/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.
β’ Bioblast editor: Plangger M β’ O2k-Network Lab: LV Riga Makrecka-Kuka M
Labels: MiParea: Respiration, Pharmacology;toxicology
Pathology: Other
Organism: Mouse Tissue;cell: Nervous system Preparation: Homogenate, Isolated mitochondria
Coupling state: LEAK, OXPHOS, ET
Pathway: N, S, NS
HRR: Oxygraph-2k, O2k-Fluorometer
2020-11, AmR