Study on effect of radix astragali on injury of cerebral cortex in neonatal rats after hypoxia/ischemia brain damage

To study the mechanism of injury of cortical nerve cell in the newborn with hypoxia/ischemia brain damage (HIBD), and the neuroprotective effect of Radix Astragali (RA). Neonatal HIBD model rats were established and divided into the sham group, the model group and the RA group. Brain of rats obtaine...

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Published inZhongguo Zhong xi yi jie he za zhi Vol. 25; no. 1; p. 54
Main Authors Jia, Rui-zhe, Jiang, Li, Qiao, Li-xing
Format Journal Article
LanguageChinese
Published China 01.01.2005
Subjects
Animals
Animals, Newborn
Apoptosis - drug effects
Astragalus membranaceus
Caspase 3
Caspases - biosynthesis
Caspases - genetics
Cell Survival
Cerebral Cortex - pathology
Drugs, Chinese Herbal - pharmacology
Female
Hypoxia-Ischemia, Brain - metabolism
Hypoxia-Ischemia, Brain - pathology
Male
Neurons - pathology
Rats
Rats, Sprague-Dawley
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
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Summary:To study the mechanism of injury of cortical nerve cell in the newborn with hypoxia/ischemia brain damage (HIBD), and the neuroprotective effect of Radix Astragali (RA). Neonatal HIBD model rats were established and divided into the sham group, the model group and the RA group. Brain of rats obtained at different time points after HIBD to conduct histopathological examination, neuron death rate count, as well as determination of caspase-3 (cysteinyl aspartate-specific proteinase-3) protein mRNA expression in cerebral cortex by immunohistochemistry, semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) respectively. In the model group, caspase-3 mRNA and protein showed an increase at 6 hrs, reached the peak at 24 hrs, and decreased at 48 hrs after HIBD, on the 5th and 7th day restored to baseline level. After being treated by RA, the neuron death rate of ligated side was obviously reduced, caspase-3 mRNA and protein expression peak value decreased by 45% (mRNA) and 40% - 43% (protein). RA
ISSN:1003-5370