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LIU Hai-juan, ZHAO Ya-ning, LI Jian-min, . Effect of Shenxionghuayu capsule on neurological function after global cerebral ischemia/reperfusion in rats[J]. Chinese Journal of Public Health, 2011, 27(4): 447-449. DOI: 10.11847/zgggws2011-27-04-29
Citation: LIU Hai-juan, ZHAO Ya-ning, LI Jian-min, . Effect of Shenxionghuayu capsule on neurological function after global cerebral ischemia/reperfusion in rats[J]. Chinese Journal of Public Health, 2011, 27(4): 447-449. DOI: 10.11847/zgggws2011-27-04-29

Effect of Shenxionghuayu capsule on neurological function after global cerebral ischemia/reperfusion in rats

  • ObjectiveTo investigate the effects of Shenxionghuayu capsule on neurological function after global cerebral ischemia/reperfusion.MethodsMale Sprague-Daw ley rats(n=40)were divided randomly into four groups:sham, model,low and high dose of Shenxionghuayu capsule treatment group.Global cerebral ischemia model was established by improved four-vessel occlusion of Pulsinelli's method.Forty-eight hours after the operation,morphological changes in hippocampal region were observed by hetatoxylin eosin(HE)staining.The quantity of apoptotic cells was measured by terminal deoxynucleotidyl transfernase medicated nick end labeling(TUNEL)method.Learning and memory function(eight-arm maze)and behavioral tests(roding method)were conducted.ResultsCompared with the sham group,the numbers of neural apoptotic cells increased(33.45±3.48)in model group.The total error times(8.94±3.78),the repeat error times (7.32±2.80),and the reference memory error times(3.48±1.26)increased.The general movement ability(79.1±24.5) decreased in model group.Compared with the model group,the number of neural apoptotic cells decreased(17.47±1.84); the total error time(3.00±1.80)and the repeat error time(2.10±0.85)decreased and the general movement ability(208.9 ±32.5)increased in Shenxionghuayu capsule group.ConclusionShenxionghuayu capsule can dramatically improve neural function after cerebral ischemia/reperfusion injury,which may be related to the suppression of neuronal apoptosis in rats.
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