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The Relationship Between The Expression Of Bcl-2,Bax Protein And Apoptosis After Cerebral Ischemia Reperfusion Injury

Posted on:2006-01-19Degree:MasterType:Thesis
Country:ChinaCandidate:L Y BaiFull Text:PDF
GTID:2144360152981745Subject:Academy of Pediatrics
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Objective: Apoptosis is a physiologically importantprocess in neurogenesis wherein approximately 50% of theneurons apoptosis during maturation of the nervous system.However, premature apoptosis and/or aberrations in apoptosiscontrol contribute to the pathogenesis of a variety ofneurological disorders such as HIV-induced encephalopathy andneurodegenerative diseases as well as ischemia reperfusioninjury. This knowledge of apoptosis mechanisms will underpinthe basis for development of new therapeutic strategies. Braindamage accompanying cardiac arrest and resuscitation isfrequent and devastating and reperfusion injury is believed torepresent one of the important factors. The mechanisms ofreperfusion injury are still not known in details. The aim of thisresearch is to study the relationship between the expression ofBcl-2,Bax protein and neuronal apoptosis after ischemiareperfusion. It may provide a method of applying genetic toolsto derive new therapies for cerebral ischemia reperfusion injury.Methods:Fifty-six male wistar rats were used in this study.The rats weighted among 180 to 220 gramme. All rats weredivided into 2 groups at random:sham-operated group,operatedgroups which were divided into 6 groups according to thedifferent time after reperfusion. Rat model of ischemiareperfusion:anesthesia was induced with 10% chloral hydrate(350mg/kg). Four-vessel occlusion(electrical coagulating bothof arteria vertebralis and ligating bilateral common carotidcortery)was used to establish the model of global cerebralischemia reperfusion in the study groups. The artery clampswere removed to recovery reperfusion after 15 minutes. Both ofarteria vertebralis and ligated bilateral common carotid arterywere not electrically coagulated in sham-operated group. Thebrain of rat was removed in 1,6,12,24,48,72hoursrespectively after reperfusion. The time-course expression ofBcl-2,Bax protein was detected in hippocampus by usingimmunohistochemical method in different time spots afterreperfusion. Meanwhile , changes of neuron apoptosis inhippocampus were detected by the TdT-mediated dUTP-biotinnick end labeling(TUNEL)method in the different time ofreperfusion. The numbers of positive neurons in hippocampalCA1 region were counted under the light microscope.Results:The number of apoptotic cells increased with thedevelopment of reperfusion within 1-48 hours and reached peakat 48h. The positive cell number was by (37.73±6.27)%,(39.61±5.97)%,(41.44±5.34)%,(70.30±4.11)% and(73.61±5.05)% respectively. The expression of Bcl-2 protein...
Keywords/Search Tags:cerebral ischemia reperfusion injury, rat, apoptosis, Bcl-2, Bax
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