Abstract |
ONO-1714, a selective inhibitor of inducible nitric oxide synthetase (iNOS) attenuated the increase of apoptosis and improved the functional outcome of urinary bladder after traumatic spinal cord injury. These findings suggest that iNOS plays a role in the process of SCI. Early treatment with 30 mg/kg methylprednisolone sodium succinate (MPSS) could also inhibit the expression of iNOS gene, apoptosis and the loss of urinary bladder function. We confirmed that early MPSS treatment may prevent injury associated with apoptosis and urinary bladder disability by reducing iNOS mRNA. However, delayed single MPSS treatment 8 h after spinal cord injury was not effective. Early repeated MPSS treatment might allow greater recovery from acute spinal cord injury.
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Authors | Yimin Yu, Yukihiro Matsuyama, Shojiro Nakashima, Makoto Yanase, Kazutoshi Kiuchi, Naoki Ishiguro |
Journal | Neuroreport
(Neuroreport)
Vol. 15
Issue 13
Pg. 2103-7
(Sep 15 2004)
ISSN: 0959-4965 [Print] England |
PMID | 15486490
(Publication Type: Comparative Study, Journal Article)
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Chemical References |
- 7-chloro-3-imino-5-methyl-2-azabicyclo(4.1.0)heptane
- Amidines
- Heterocyclic Compounds, 2-Ring
- Neuroprotective Agents
- RNA, Messenger
- Methylprednisolone Hemisuccinate
- Nitric Oxide Synthase
- Nitric Oxide Synthase Type II
- Nos2 protein, rat
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Topics |
- Amidines
(therapeutic use)
- Animals
- Cell Count
(methods)
- Cell Death
(drug effects)
- Drug Interactions
- Gene Expression Regulation
(drug effects)
- Heterocyclic Compounds, 2-Ring
(therapeutic use)
- Immunohistochemistry
(methods)
- In Situ Nick-End Labeling
(methods)
- Male
- Methylprednisolone Hemisuccinate
(therapeutic use)
- Neuroprotective Agents
(therapeutic use)
- Nitric Oxide Synthase
(antagonists & inhibitors, genetics, metabolism)
- Nitric Oxide Synthase Type II
- RNA, Messenger
(biosynthesis)
- Rats
- Rats, Sprague-Dawley
- Reverse Transcriptase Polymerase Chain Reaction
(methods)
- Spinal Cord Injuries
(complications, drug therapy, enzymology)
- Time Factors
- Urinary Bladder, Neurogenic
(drug therapy, etiology)
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