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2009 | 69 | 4 |
Tytuł artykułu

Thalidomide fails to be therapeutic following contusive spinal cord injury in rats

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Mechanical damage to the spinal cord (SC) generates self-destructive processes that contribute to post-traumatic neurodegeneration. Because thalidomide apparently counteracts these effects its use clinically has been proposed enthusiastically. Nonetheless, we tested its action as a neuroprotectant in a clinically relevant model of SC injury in rats. We administered thalidomide intraperitoneally to rats subjected to thoracic SC contusion as single or repeated doses within the first 24 h after injury. Edema, neutrophil infiltration, and cord tissue preservation/destruction were assessed in the SC 24 h after injury and motor function for 7 weeks. Rats treated with thalidomide showed significant increase in SC water compared with naïve rats, but not vehicle-treated rats; their neutrophil infiltration and amount of spared/destroyed cord tissue was not different from vehicle-treated rats; and in no case was motor performance improved after thalidomide. In conclusion, thalidomide failed here to be therapeutic, discouraging its use clinically for SC trauma.
Słowa kluczowe
Wydawca
-
Rocznik
Tom
69
Numer
4
Opis fizyczny
p.494–503,fig.,ref.
Twórcy
  • Research Unit for Neurological Diseases, Medical Center Century XXI, Mexican Social Security Institute, Mexico City, Mexico
  • Department of Surgery, School of Veterinary Medicine, Autonomous University of the State of Mexico, Toluca, Mexico
  • Department of Experimental Surgery, Camina Project A.C., Mexico City, Mexico
  • Department of Biochemistry, National Institute for Rehabilitation, Mexico City, Mexico
  • Department of Experimental Surgery, Camina Project A.C., Mexico City, Mexico
autor
  • Research Unit for Neurological Diseases, Medical Center Century XXI, Mexican Social Security Institute, Mexico City, Mexico
  • Department of Experimental Surgery, Camina Project A.C., Mexico City, Mexico
autor
  • Department of Experimental Surgery, Camina Project A.C., Mexico City, Mexico
autor
  • Research Unit for Neurological Diseases, Medical Center Century XXI, Mexican Social Security Institute, Mexico City, Mexico
  • Department of Experimental Surgery, Camina Project A.C., Mexico City, Mexico
  • Research Unit for Neurological Diseases, Medical Center Century XXI, Mexican Social Security Institute, Mexico City, Mexico
  • Department of Experimental Surgery, Camina Project A.C., Mexico City, Mexico
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