Treatment of spinal cord impact injury in the XXXX with transforming growth factor-beta.

@entity35 @entity1505 @entity1810 @entity1566 @entity130
To investigate the contribution of cytokines, proinflammatory @entity1505 and inhibitory @entity1810 , to @entity1566 ( @entity1566 ) in a @entity35 model, two studies were performed using adult @entity35 which were injured at T9/T10. In the first study, @entity35 were sacrificed at 1, 6, 24, 96 and 168 h after @entity1566 for immunocytochemistry of coronal sections for the presence of mononuclear phagocytes, astrocytes, @entity1505 and @entity1810 , among other markers. From intervening frozen sections, RNA was extracted for semiquantitative polymerase chain reaction (RT-PCR) analysis of @entity1505 and @entity1810 . In the second experiment, @entity35 were treated with intravenous @entity1810 30 min after injury and sacrificed at 6 and 48 h after injury. Spinal cord sections were immunocytochemically stained and RNA extracted for semiquantitative PCR as mentioned above, as well as quantitation of lesion volume. There were increases in mononuclear phagocytes and astrocytes, as early as 1 h after @entity1566 , with steady progression over 168 h after injury. @entity1505 and @entity1810 was produced locally by mononuclear phagocytes and astrocytes. There was an 18-h delay in peak mRNA production of @entity1810 compared to @entity1505 . The treatment of @entity1566 @entity35 with @entity1810 reduced lesion volume by 50% at 48 h and this was associated with decreased accumulation of mononuclear phagocytes in and around the injury site. This reduction of mononuclear phagocyte numbers around the site of @entity130 would reduce their contribution to secondary injury.
