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Titolo:
Paradoxical increase in neuronal DNA fragmentation after neuroprotective free radical scavenger treatment in experimental traumatic brain injury
Autore:
Lewen, A; Skoglosa, Y; Clausen, F; Marklund, N; Chan, PH; Lindholm, D; Hillered, L;
Indirizzi:
Univ Uppsala Hosp, Div Neurosurg, Dept Neurosci, SE-75185 Uppsala, Sweden Univ Uppsala Hosp Uppsala Sweden SE-75185 osci, SE-75185 Uppsala, Sweden Univ Uppsala Hosp, Dept Med Sci Clin Chem, SE-75185 Uppsala, Sweden Univ Uppsala Hosp Uppsala Sweden SE-75185 Chem, SE-75185 Uppsala, Sweden Ctr Biomed, Div Neurobiol, Dept Neurosci, Uppsala, Sweden Ctr Biomed Uppsala Sweden Div Neurobiol, Dept Neurosci, Uppsala, Sweden Stanford Univ, Sch Med, Dept Neurosurg, Palo Alto, CA 94304 USA Stanford Univ Palo Alto CA USA 94304 t Neurosurg, Palo Alto, CA 94304 USA Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Palo Alto, CA 94304 USA Stanford Univ Palo Alto CA USA 94304 Neurol Sci, Palo Alto, CA 94304 USA Stanford Univ, Sch Med, Program Neurosci, Palo Alto, CA 94304 USA StanfordUniv Palo Alto CA USA 94304 am Neurosci, Palo Alto, CA 94304 USA
Titolo Testata:
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
fascicolo: 4, volume: 21, anno: 2001,
pagine: 344 - 350
SICI:
0271-678X(200104)21:4<344:PIINDF>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
TERT-BUTYL NITRONE; APOPTOTIC CELL-DEATH; RAT-BRAIN; DELAYED TREATMENT; CONTUSION TRAUMA; NECROSIS; PBN; DYSFUNCTION; ACTIVATION; DEFICITS;
Keywords:
traumatic brain injury; cell death; apoptosis; necrosis; behavior; Outcome; caspases;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Hillered, L Univ Uppsala Hosp, Div Neurosurg, Dept Neurosci, SE-75185 Uppsala, Sweden Univ Uppsala Hosp Uppsala Sweden SE-75185 85 Uppsala, Sweden
Citazione:
A. Lewen et al., "Paradoxical increase in neuronal DNA fragmentation after neuroprotective free radical scavenger treatment in experimental traumatic brain injury", J CEREBR B, 21(4), 2001, pp. 344-350

Abstract

The mechanisms and role of nerve cell death after traumatic brain injury (TBI) are not fully understood. The authors investigated the effect of pretreatment with the oxygen free radical spin trap alpha -phenyl-N-tert-butyl-nitrone (PBN) on the number of neurons undergoing apoptosis after TBI in rats. Apoptotic cells were identified by the TUNEL method combined with the nuclear stain, Hoechst 33258, and immunohistochemistry for the active form ofcaspase-3. Numerous neurons became positive for activated caspase-3 and TUNEL in the cortex at 24 hours after injury, suggesting ongoing biochemical apoptosis. In PBN-treated rats, a significantly greater number of cells were found to be TUNEL positive at 24 hours compared with controls. However, PEN treatment resulted in a reduced cortical lesion volume and improved behavioral outcome two weeks after injury. The authors conclude that a treatment producing an increase in DNA fragmentation in the early phase may be compatible with an overall beneficial effect on outcome after TBI. This should be considered in the screening process for future neuroprotective remedies.

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Documento generato il 02/07/20 alle ore 19:07:49