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

Abstract

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 naive 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.

• Authors: Horacio J Reyes-Alva, Rebecca E Franco-Bourland, Angelina Martínez-Cruz, Israel Grijalva, Bruno Fuchs, Ignacio Madrazo, Gabriel Guízar-Sahagún
• Journal: Acta neurobiologiae experimentalis (Acta Neurobiol Exp (Wars)) Vol. 69 Issue 4 Pg. 494-503 ( 2009) ISSN: 0065-1400 [Print] Poland
• PMID: 20048765 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Immunosuppressive Agents
• Thalidomide

Topics

• Analysis of Variance
• Animals
• Disease Models, Animal
• Dose-Response Relationship, Drug
• Edema (etiology)
• Female
• Immunosuppressive Agents (therapeutic use)
• Locomotion (drug effects, physiology)
• Neutrophils (drug effects)
• Rats
• Rats, Long-Evans
• Spinal Cord Injuries (complications, drug therapy)
• Thalidomide (therapeutic use)
• Time Factors