Abstract
This study was undertaken to examine the effect of transforming growth factor-beta 1 (TGF-beta 1) administered into the subarachnoid space after spinal cord injury (SCI) on the increased production of inducible-nitric oxide synthase (i-NOS) in the injured spinal cord in rats. The expression of i-NOS mRNA after SCI was remarkably down-regulated by TGF-beta 1 in vivo. Rats treated with TGF-beta 1 showed a better outcome regarding hindlimb motor dysfunction in the first 5 days after injury compared to the saline-treated rats. However, the final outcome was not better and fibrous scar formation in the injured spinal cord was more evident, which was demonstrated as increased immunoreactivity of fibronectin in the later stage after SCI. These results provide evidence of both positive and negative contributions of TGF-beta 1 to the pathology associated with SCI.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
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Cicatrix / pathology
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Depression, Chemical
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Drug Evaluation, Preclinical
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Enzyme Induction / drug effects
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Fibronectins / analysis
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Injections, Spinal
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Male
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Nerve Regeneration / drug effects
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Nitric Oxide / biosynthesis
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Nitric Oxide Synthase / biosynthesis
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Paresis / etiology
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Paresis / prevention & control
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RNA, Messenger / biosynthesis
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Rats
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Rats, Wistar
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Spinal Cord Injuries / complications
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Spinal Cord Injuries / drug therapy*
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Spinal Cord Injuries / metabolism
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Spinal Cord Injuries / pathology
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Subarachnoid Space
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Transforming Growth Factor beta / pharmacology
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Transforming Growth Factor beta / therapeutic use*
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Fibronectins
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RNA, Messenger
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Transforming Growth Factor beta
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Nitric Oxide
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Nitric Oxide Synthase