الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
SCI often results in irreversible and permanent neurological deficits below the injury site and is considered a pathological state of functional damage to local neurons and axons fibres. Actually there are few therapeutic treatments to minimize tissue damage and promote repair in spinal cord. After SCI a cascade of cellular events occurs, including the early activation of inflammatory cytokines, and glial cyst and scar formation in the following days: in particular glial cells can produce chemokines and cytokines [such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin -6 (IL-6)] which mediate the recruitment of inflammatory cells to the injury site. Indeed blocking these molecules could represent a potential therapeutic strategy in the treatment of acute SCI. To this aim, one could prevent either the production or the release of inflammatory molecules.