RS-Glucoraphanin bioactivated with myrosinase treatment counteracts proinflammatory cascade and apoptosis associated to spinal cord injury in an experimental mouse model.

Spinal cord injury (SCI) is a highly debilitating pathology. Although innovative medical care has been improved, drug therapies to counteract neuronal damage and promote regeneration are limited. An experimental mouse model of SCI was designed to examine the possible neuroprotective role of the glucosinolate (RS)-glucoraphanin (RS-GRA), bioactivated with myrosinase enzyme (MYR-activated RS-GRA). Methodologically, the injury was induced by application of an aneurysm clip (force of 24 g) for 1 min via four-level T5-T8 after laminectomy. MYR-activated RS-GRA was administered in mice (10mg/kg i.p.) 1 and 6h after the trauma, identified as the therapeutic intervention window. The treatment with MYR-activated RS-GRA significantly decreased histological damage resulted by proinflammatory events as well as by apoptosis cascade. Overall, by quantitative analysis of immunohistochemical images, the neuroprotection has been quite evident. MYR-activated RS-GRA has given a histological quantification around zero in all determinations. Particularly, looking at the strongest data obtained, regarding the glial fibrillary acidic protein (GFAP), result the high tissue localization of this damage marker mediated by astrocyte activity, estimated as about 80% of positive staining, was shot down by MYR-activated RS-GRA treatment. Taken together, our results show that MYR-activated RS-GRA could represent an interesting approach for the management of secondary damage following SCI.
AuthorsMaria Galuppo, Sabrina Giacoppo, Gina Rosalinda De Nicola, Renato Iori, Emanuela Mazzon, Placido Bramanti
JournalJournal of the neurological sciences (J Neurol Sci) Vol. 334 Issue 1-2 Pg. 88-96 (Nov 15 2013) ISSN: 1878-5883 [Electronic] Netherlands
PMID23992921 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2013 Elsevier B.V. All rights reserved.
Chemical References
  • Glucosinolates
  • Imidoesters
  • Inflammation Mediators
  • Neuroprotective Agents
  • glucoraphanin
  • Glycoside Hydrolases
  • thioglucosidase
  • Animals
  • Apoptosis (drug effects)
  • Disease Models, Animal
  • Enzyme Activation (drug effects)
  • Glucosinolates (metabolism, therapeutic use)
  • Glycoside Hydrolases (therapeutic use)
  • Imidoesters (metabolism, therapeutic use)
  • Inflammation Mediators (metabolism)
  • Male
  • Mice
  • Neuroprotective Agents (pharmacology, therapeutic use)
  • Spinal Cord Injuries (drug therapy, metabolism, pathology)
  • Thoracic Vertebrae (injuries)

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