Methylprednisolone treatment delays remote cell death after focal brain lesion (Articolo in rivista)

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  • Methylprednisolone treatment delays remote cell death after focal brain lesion (Articolo in rivista) (literal)
Anno
  • 2008-01-01T00:00:00+01:00 (literal)
Alternative label
  • Viscomi M.T.1; Florenzano F.1,2; Latini L. 1; Amantea D. 1,3; Bernardi G. 1, 4; Molinari M. 1 (2008)
    Methylprednisolone treatment delays remote cell death after focal brain lesion
    in Neuroscience
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Viscomi M.T.1; Florenzano F.1,2; Latini L. 1; Amantea D. 1,3; Bernardi G. 1, 4; Molinari M. 1 (literal)
Pagina inizio
  • 1267 (literal)
Pagina fine
  • 1282 (literal)
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  • Impact Factor 3,3 (literal)
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  • 154/4 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1 = Santa Lucia Foundation Istituto Ricovero e Cura Carattere Scientifico (I.R.C.C.S.), Via del Fosso di Fiorano 65, 00143 Rome, Italy 2 = CNR INMM, Via del Fosso di Fiorano 65, 00143 Rome, Italy; 3 = Department of Pharmacobiology, University of Calabria, Via P. Bucci, Ed. Polifunzionale, 87036 Arcavacata di Rende (CS), Italy; 4 = Department of Neuroscience, University of Rome “Tor Vergata,” Viale Oxford 81, 00133 Rome, Italy (literal)
Titolo
  • Methylprednisolone treatment delays remote cell death after focal brain lesion (literal)
Abstract
  • Glucocorticoids have a prominent role in the treatment of CNS injuries. However, the cellular consequences of glucocorticoid treatment on remote degenerative responses after focal brain lesions have been poorly investigated. Here we examine the effectiveness of a high dose (50 mg/kg) of methylprednisolone sodium succinate (MPSS) in reducing neuronal loss, glial response and glial-derived inflammatory mediators in inferior olive and pontine nuclei after lesion of the contralateral cerebellar hemisphere using immunohistochemistry and Western blot techniques. Quantitative analysis demonstrated that MPSS treatment significantly improved the survival of neurons in remote precerebellar stations. This survival was accompanied by reduction in the postlesional activation of microglia, astrocytes and interleukin-1 beta (IL-1²). Cell death resumed after suspension of MPSS treatment and this delayed wave of cell loss was paralleled by reactivation of the inflammatory markers analyzed. The present study confirms the importance of inflammatory events in inducing remote cell death and that this type of degeneration can be delayed by MPSS treatment. Furthermore, the sustained effect of MPSS treatment, up to 28 days postlesion, and the reactivation of the degenerative phenomena after its suspension, support the hypothesis that glucocorticoid treatment, although capable of delaying cell death mechanisms, is not effective in blocking the cascade of remote degenerative events started by the primary lesion. (literal)
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