Abstract | BACKGROUND: METHODS: Rats were divided at random into three groups. The first group received 1 mL of saline ( contusion + saline group, n = 5). Rats of the second group were treated with 3000 IU/kg of PC-SOD ( contusion + SOD 1 group, n = 5), while the third group received 5000 IU/kg of PC-SOD ( contusion + SOD 2 group, n = 5). All agents were administered intraperitoneally 1 minute after traumatic insult and every 24 hours until 2 or 3 days post-TBI. Animals were sacrificed 3 or 7 days after contusion injury. RESULTS: PC-SOD prevented CA3 neuronal loss 3 days after TBI, and increased the number of surviving CA3 neurons 7 days after TBI. CONCLUSION: Our findings suggest that PC-SOD may serve as a pharmacological agent in the treatment of neuronal loss after TBI.
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Authors | Masatoshi Yunoki, Masamitsu Kawauchi, Naoya Ukita, Tomoyuki Sugiura, Takashi Ohmoto |
Journal | Surgical neurology
(Surg Neurol)
Vol. 59
Issue 3
Pg. 156-60; discussion 160-1
(Mar 2003)
ISSN: 0090-3019 [Print] United States |
PMID | 12681536
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Phosphatidylcholines
- Superoxide Dismutase
- lecithinized superoxide dismutase
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Topics |
- Animals
- Brain Injuries
(complications, drug therapy, pathology)
- Cell Count
- Disease Models, Animal
- Dose-Response Relationship, Drug
- Drug Administration Schedule
- Hippocampus
(drug effects, injuries, pathology)
- Male
- Nerve Degeneration
(etiology, pathology, prevention & control)
- Phosphatidylcholines
(administration & dosage, therapeutic use)
- Rats
- Rats, Sprague-Dawley
- Superoxide Dismutase
(administration & dosage, therapeutic use)
- Time Factors
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