Abstract
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 24g) for 1 min via four-level T5-T8 after laminectomy. MYR-activated RS-GRA was administered in mice (10 mg/kg i.p.) 1 and 6 h after the trauma, identified as the therapeutic intervention window. The treatment with MYR-activated R S-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.
| Original language | English |
|---|---|
| Pages (from-to) | 88-96 |
| Number of pages | 9 |
| Journal | Journal of the Neurological Sciences |
| Volume | 334 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Nov 15 2013 |
Fingerprint
Keywords
- Apoptosis
- Bioactive (R)-glucoraphanin
- Inflammation
- Myrosinase enzyme
- Proinflammatory cytokines
- Spinal cord injury
ASJC Scopus subject areas
- Clinical Neurology
- Neurology
Cite this
RS-Glucoraphanin bioactivated with myrosinase treatment counteracts proinflammatory cascade and apoptosis associated to spinal cord injury in an experimental mouse model. / Galuppo, Maria; Giacoppo, Sabrina; De Nicola, Gina Rosalinda; Iori, Renato; Mazzon, Emanuela; Bramanti, Placido.
In: Journal of the Neurological Sciences, Vol. 334, No. 1-2, 15.11.2013, p. 88-96.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - RS-Glucoraphanin bioactivated with myrosinase treatment counteracts proinflammatory cascade and apoptosis associated to spinal cord injury in an experimental mouse model
AU - Galuppo, Maria
AU - Giacoppo, Sabrina
AU - De Nicola, Gina Rosalinda
AU - Iori, Renato
AU - Mazzon, Emanuela
AU - Bramanti, Placido
PY - 2013/11/15
Y1 - 2013/11/15
N2 - 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 24g) for 1 min via four-level T5-T8 after laminectomy. MYR-activated RS-GRA was administered in mice (10 mg/kg i.p.) 1 and 6 h after the trauma, identified as the therapeutic intervention window. The treatment with MYR-activated R S-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.
AB - 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 24g) for 1 min via four-level T5-T8 after laminectomy. MYR-activated RS-GRA was administered in mice (10 mg/kg i.p.) 1 and 6 h after the trauma, identified as the therapeutic intervention window. The treatment with MYR-activated R S-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.
KW - Apoptosis
KW - Bioactive (R)-glucoraphanin
KW - Inflammation
KW - Myrosinase enzyme
KW - Proinflammatory cytokines
KW - Spinal cord injury
UR - http://www.scopus.com/inward/record.url?scp=84887465716&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84887465716&partnerID=8YFLogxK
U2 - 10.1016/j.jns.2013.07.2514
DO - 10.1016/j.jns.2013.07.2514
M3 - Article
VL - 334
SP - 88
EP - 96
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
SN - 0022-510X
IS - 1-2
ER -