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Titolo:
Methylprednisolone reduces spinal cord injury in rats without affecting tumor necrosis factor-alpha production
Autore:
Taoka, Y; Okajima, K; Uchiba, M; Johno, M;
Indirizzi:
Kumamoto Univ, Sch Med, Dept Lab Med, Kumamoto 8600811, Japan Kumamoto Univ Kumamoto Japan 8600811 pt Lab Med, Kumamoto 8600811, Japan Kumamoto Univ, Sch Med, Dept Dermatol, Kumamoto 8600811, Japan Kumamoto Univ Kumamoto Japan 8600811 t Dermatol, Kumamoto 8600811, Japan
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 5, volume: 18, anno: 2001,
pagine: 533 - 543
SICI:
0897-7151(200105)18:5<533:MRSCII>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
POLYMORPHONUCLEAR LEUKOCYTES; LIPID-PEROXIDATION; MESSENGER-RNA; EXPRESSION; COMPRESSION; MICROCIRCULATION; DEXAMETHASONE; EXTRAVASATION; NEUTROPHILS; INHIBITION;
Keywords:
accumulation of leukocytes; lipid peroxidation; methylprednisolone; motor disturbance; spinal cord injury; tumor necrosis factor-alpha; vascular permeability;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Okajima, K Kumamoto Univ, Sch Med, Dept Lab Med, Honjo 1-1-1, Kumamoto 8600811, Japan Kumamoto Univ Honjo 1-1-1 Kumamoto Japan 8600811 600811, Japan
Citazione:
Y. Taoka et al., "Methylprednisolone reduces spinal cord injury in rats without affecting tumor necrosis factor-alpha production", J NEUROTRAU, 18(5), 2001, pp. 533-543

Abstract

Methylprednisolone (MPS) is the only therapeutic agent currently availablefor traumatic spinal cord injury (SCI). However, little is known about itstherapeutic mechanisms. We have demonstrated that tumor necrosis factor-alpha (TNF-alpha) plays a critical role in posttraumatic SCI in rats. Since MPS has been shown to inhibit TNF-alpha production in vitro, it is possible that MPS can reduce SCI by inhibiting TNF-alpha production. To examine thispossibility, we investigated the effect of MPS on TNF-alpha production in injured segments of rat spinal cord. Leukocytopenia and high-dose intravenous administration of MPS markedly reduced the motor disturbances observed following spinal cord trauma. Both treatments also reduced the intramedullary hemorrhages observed histologically 24 hr posttrauma. Leukocytopenia significantly reduced tissue levels of both TNF-alpha mRNA and TNF-alpha, 1 and4 hr posttrauma, respectively, and it also inhibited the accumulation of leukocytes in the injured segments 3 hr posttrauma, while MPS had no effects. Lipid peroxidation and vascular permeability at the site of spinal cord lesion were both significantly increased over time after the induction of SCI, peaking 3 hr posttrauma. These events were significantly reduced in animals with leukocytopenia and in those given anti-P-selectin monoclonal antibody compared to sham-operated animals. Administration of MPS significantly inhibited both the increase in lipid peroxidation and the vascular permeability. These findings suggested that MPS reduces the severity of SCI, not byinhibiting the production of TNF-alpha at the site of spinal cord trauma, but by inhibiting activated leukocyte induced lipid peroxidation of the endothelial cell membrane. This suggests that MPS may attenuate spinal cord ischemia by inhibiting the increase in endothelial permeability at the site of spinal cord injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 20:40:57