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a teraz na szybko wpadlo mi toto
Creatine-enhanced diet alters levels of lactate and free fatty acids after experimental brain injury.
Scheff SW, Dhillon HS.
Sanders-Brown Center on Aging, University of Kentucky, 101 Sanders-Brown, University of Kentucky, Lexington, Kentucky 40536-0230, USA. [email protected]
Free fatty acids (FFA) and lactic acid are markers of secondary cellular injury following traumatic brain injury (TBI). We previously showed that animals fed a creatine (Cr)-enriched diet are afforded neuroprotection following TBI. To further characterize the neuroprotective Cr diet, we studied neurochemical changes in cortex and hippocampus following a moderate injury. Adult rats were fed either a control or Cr-supplemented diet (0.5%, 1%) for 2 weeks before TBI. At 30 min or 6 h after injury, tissue was processed for quantitative analysis of neurochemical changes. Both lactate and FFA were significantly increased in all tissues ipsilateral to the injury. Cr-fed animals had significantly lower levels, although the levels were elevated compared to sham controls. Animals fed a 1% Cr-diet were afforded greater neuroprotection than animals fed a 0.5% Cr diet. These results support the idea that a Cr-enriched diet can provide substantial neuroprotection in part by suppressing secondary brain injury.
Creatine diet supplement for spinal cord injury: influences on functional recovery and tissue sparing in rats.
Rabchevsky AG, Sullivan PG, Fugaccia I, Scheff SW.
Sanders-Brown Center on Aging, Department of Physiology, University of Kentucky, 236 Health Sciences Research Building, Lexington, Kentucky 40536-0305, USA. [email protected]
Creatine-supplemented diet significantly attenuates cortical damage after traumatic brain injury in rodents. The protective mechanism likely involves maintenance of mitochondrial homeostasis. In the present study, we used two separate contusion spinal cord injury (SCI) instruments--the NYU device and the PSI Infinite Horizon (IH) impactor--to assess the efficacy of creatine-supplemented diets on hind limb functional recovery and tissue sparing in adult rats. Rats were fed control versus 2% creatine-supplemented chow for 4-5 weeks prior to SCI (pre-fed), after which most resumed a control diet while some remained on a 2% creatine diet (pre & post-fed). Following long-term behavioral analysis (BBB), the amount of spared spinal cord tissue among the dietary regimen groups was assessed using stereology. Comparatively, both instruments caused similar amounts of gray matter damage while the NYU device rendered a greater loss of white matter, reflected in more severe hind limb functional deficits than with the IH impactor. Relative to the control fed groups injured with either instrument, none of the creatine fed animals showed improvements in hind limb function or white matter tissue sparing. Although creatine did not attenuate gray matter loss in the NYU cohort, it significantly spared gray matter in the IH cohort with pre-fed and pre & post-fed regimens. Such selective sparing of injured spinal cord gray matter with a dietary supplement yields a promising strategy to promote neuroprotection after SCI. The relationship between the efficacy of creatine and the magnitude of the insults is discussed.
a to chyba bylo zrodlo poczatkowego arta -
Dietary supplement creatine protects against traumatic brain injury.
Sullivan PG, Geiger JD, Mattson MP, Scheff SW.
Sanders-Brown Center on Aging, University of Kentucky, Lexington 40536-0230, USA.
Creatine, one of the most common food supplements used by individuals at almost every level of athleticism, promote gains in performance, strength, and fat-free mass. Recent experimental findings have demonstrated that creatine affords significant neuroprotection against ischemic and oxidative insults. The present experiments investigated the possible effect of creatine dietary supplementation on brain tissue damage after experimental traumatic brain injury. Results demonstrate that chronic administration of creatine ameliorated the extent of cortical damage by as much as 36% in mice and 50% in rats. Protection seems to be related to creatine-induced maintenance of mitochondrial bioenergetics. Mitochondrial membrane potential was significantly increased, intramitochondrial levels of reactive oxygen species and calcium were significantly decreased, and adenosine triphosphate levels were maintained. Induction of mitochondrial permeability transition was significantly inhibited in animals fed creatine. This food supplement may provide clues to the mechanisms responsible for neuronal loss after traumatic brain injury and may find use as a neuroprotective agent against acute and delayed neurodegenerative processes.
a teraz na szybko wpadlo mi toto
Creatine-enhanced diet alters levels of lactate and free fatty acids after experimental brain injury.
Scheff SW, Dhillon HS.
Sanders-Brown Center on Aging, University of Kentucky, 101 Sanders-Brown, University of Kentucky, Lexington, Kentucky 40536-0230, USA. [email protected]
Free fatty acids (FFA) and lactic acid are markers of secondary cellular injury following traumatic brain injury (TBI). We previously showed that animals fed a creatine (Cr)-enriched diet are afforded neuroprotection following TBI. To further characterize the neuroprotective Cr diet, we studied neurochemical changes in cortex and hippocampus following a moderate injury. Adult rats were fed either a control or Cr-supplemented diet (0.5%, 1%) for 2 weeks before TBI. At 30 min or 6 h after injury, tissue was processed for quantitative analysis of neurochemical changes. Both lactate and FFA were significantly increased in all tissues ipsilateral to the injury. Cr-fed animals had significantly lower levels, although the levels were elevated compared to sham controls. Animals fed a 1% Cr-diet were afforded greater neuroprotection than animals fed a 0.5% Cr diet. These results support the idea that a Cr-enriched diet can provide substantial neuroprotection in part by suppressing secondary brain injury.
Creatine diet supplement for spinal cord injury: influences on functional recovery and tissue sparing in rats.
Rabchevsky AG, Sullivan PG, Fugaccia I, Scheff SW.
Sanders-Brown Center on Aging, Department of Physiology, University of Kentucky, 236 Health Sciences Research Building, Lexington, Kentucky 40536-0305, USA. [email protected]
Creatine-supplemented diet significantly attenuates cortical damage after traumatic brain injury in rodents. The protective mechanism likely involves maintenance of mitochondrial homeostasis. In the present study, we used two separate contusion spinal cord injury (SCI) instruments--the NYU device and the PSI Infinite Horizon (IH) impactor--to assess the efficacy of creatine-supplemented diets on hind limb functional recovery and tissue sparing in adult rats. Rats were fed control versus 2% creatine-supplemented chow for 4-5 weeks prior to SCI (pre-fed), after which most resumed a control diet while some remained on a 2% creatine diet (pre & post-fed). Following long-term behavioral analysis (BBB), the amount of spared spinal cord tissue among the dietary regimen groups was assessed using stereology. Comparatively, both instruments caused similar amounts of gray matter damage while the NYU device rendered a greater loss of white matter, reflected in more severe hind limb functional deficits than with the IH impactor. Relative to the control fed groups injured with either instrument, none of the creatine fed animals showed improvements in hind limb function or white matter tissue sparing. Although creatine did not attenuate gray matter loss in the NYU cohort, it significantly spared gray matter in the IH cohort with pre-fed and pre & post-fed regimens. Such selective sparing of injured spinal cord gray matter with a dietary supplement yields a promising strategy to promote neuroprotection after SCI. The relationship between the efficacy of creatine and the magnitude of the insults is discussed.
a to chyba bylo zrodlo poczatkowego arta -
Dietary supplement creatine protects against traumatic brain injury.
Sullivan PG, Geiger JD, Mattson MP, Scheff SW.
Sanders-Brown Center on Aging, University of Kentucky, Lexington 40536-0230, USA.
Creatine, one of the most common food supplements used by individuals at almost every level of athleticism, promote gains in performance, strength, and fat-free mass. Recent experimental findings have demonstrated that creatine affords significant neuroprotection against ischemic and oxidative insults. The present experiments investigated the possible effect of creatine dietary supplementation on brain tissue damage after experimental traumatic brain injury. Results demonstrate that chronic administration of creatine ameliorated the extent of cortical damage by as much as 36% in mice and 50% in rats. Protection seems to be related to creatine-induced maintenance of mitochondrial bioenergetics. Mitochondrial membrane potential was significantly increased, intramitochondrial levels of reactive oxygen species and calcium were significantly decreased, and adenosine triphosphate levels were maintained. Induction of mitochondrial permeability transition was significantly inhibited in animals fed creatine. This food supplement may provide clues to the mechanisms responsible for neuronal loss after traumatic brain injury and may find use as a neuroprotective agent against acute and delayed neurodegenerative processes.
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