Linked Life Data

16725128

Source:http://linkedlifedata.com/resource/pubmed/id/16725128

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-6-19
pubmed:abstractText
Neuronal cell damage following hypoxic-ischemic (HI) brain injury is partly caused by production of free radicals and reactive oxygen species (ROS). Ascorbic acid (AA) is a potent antioxidant, which scavenges various types of ROS. Some studies have shown that it is neuroprotective, however, the issue is still controversial. In this study, we examined the effect of intraventricular AA administration on immature HI brain using the Rice-Vannucci model. After unilateral carotid artery ligation under isoflurane anesthesia, 7-day-old rat pups received varying concentrations of AA (0.04, 0.2, 1 and 5 mg/kg) by intraventricular injection and were exposed to 8% oxygen for 90 min. Vehicle controls received an equal volume of phosphate saline buffer. We assessed the neuroprotective effect of AA at 7 days post-HI. The percent brain damage measured by comparing the wet weight of the ligated side of hemisphere with that of contralateral one was reduced in both 1 and 5 mg/kg groups but not in either 0.04 or 0.2 mg/kg groups compared to vehicle controls (5 mg/kg 16.0 +/- 4.3%, 1 mg/kg 10.9 +/- 5.0%, vs. controls 36.7 +/- 3.6%, P < 0.05). Macroscopic evaluation of brain injury revealed the neuroprotective effect of AA in both 1 and 5 mg/kg groups (5 mg/kg 1.1 +/- 0.4, 1 mg/kg 0.4 +/- 0.3, vs. controls 2.9 +/- 0.3, P < 0.05). Western blots of fodrin on the ligated side also showed that AA significantly suppressed 150/145-kDa bands of fodrin breakdown products, which suggested that AA suppressed activation of calpain. Neuropathological quantitative analysis of cell death revealed that 1 mg/kg of AA injection significantly reduced the number of necrotic cells in cortex, caudate putamen, thalamus and hippocampus CA1, whereas that of apoptotic cells was only reduced in cortex. These findings show that intraventricular AA injection is neuroprotective after HI in immature rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
1095
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
159-66
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16725128-Analysis of Variance, pubmed-meshheading:16725128-Animals, pubmed-meshheading:16725128-Animals, Newborn, pubmed-meshheading:16725128-Antioxidants, pubmed-meshheading:16725128-Apoptosis, pubmed-meshheading:16725128-Ascorbic Acid, pubmed-meshheading:16725128-Blotting, Western, pubmed-meshheading:16725128-Body Weight, pubmed-meshheading:16725128-Carrier Proteins, pubmed-meshheading:16725128-Cell Count, pubmed-meshheading:16725128-Functional Laterality, pubmed-meshheading:16725128-Hypoxia, Brain, pubmed-meshheading:16725128-Hypoxia-Ischemia, Brain, pubmed-meshheading:16725128-Injections, Intraventricular, pubmed-meshheading:16725128-Microfilament Proteins, pubmed-meshheading:16725128-Molecular Weight, pubmed-meshheading:16725128-Necrosis, pubmed-meshheading:16725128-Organ Size, pubmed-meshheading:16725128-Rats, pubmed-meshheading:16725128-Rats, Wistar
pubmed:year
2006
pubmed:articleTitle
Intraventricular ascorbic acid administration decreases hypoxic-ischemic brain injury in newborn rats.
pubmed:affiliation
Department of Pediatrics, Akita University School of Medicine, 1-1-1 Hondo, Akita, 010-8543, Japan. miurash@doc.med.akita-u.ac.jp
pubmed:publicationType
Journal Article, Comparative Study