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Apoptosis Inducing Factor and Hypoxic-ischemic Brain Injury in the Immature Brain

Author: HuangZhiHeng
Tutor: ZhuChangLian；ChengXiuYong
School: Zhengzhou University
Course: Pediatrics
Keywords: Apoptosis-inducing factor Radicals Hypoxic-ischemic Brain
CLC: R722.1
Type: Master's thesis
Year: 2007
Downloads: 56
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Abstract

The purpose of neonatal hypoxic-ischemic brain injury (HI) sex is one of the important reasons leading to neonatal death and disability of children, the complex pathogenesis involves a number of aspects, including free radical damage, caspase enzyme (caspase) activation and apoptosis-inducing factor (AIF) release and nuclear transfer. This study investigated the AIF down as well as joint application radical scavenger Edaravone (3 - methyl-1-phenyl-2 - pyrazolin-5 - one) immature hypoxic-ischemic brain injury. Object (1) the observed HI male wild-type (Wt) mice and Hq mice brain injury: the 9-day-old male Wt mice Hq same-day-old male mice (n = 37) (n = 33), HI 72h after the assessment of the degree of brain damage. (2) concept Chayidala the Bong Wt mice and Hq mice brain injury protection situation: 9-day-old Wt mice in the control group (n = 16) and edaravone treatment group (n = 17), 9, 2011 age Hq mice in the control group (n = 17) and edaravone treatment group (n = 16) after 72h after HI assessment of the degree of brain damage. (3) observation of calpain half caspase 3 activity: each 6 Wt mice and Hq mice of the same age, HI Wt mice after 24h and Hq mice brain homogenates, immunization blot and caspase activity was measured. (4) Wt mice control group and edaravone six each treatment group, the the Hq mice control group and edaravone treated group 6 h after HI, 24h reperfusion brain immunohistochemical staining. Method 1 neonatal mouse HI brain injury animal model preparation: 9 days after birth, the newborn mice ligation of the left common carotid artery and inhaled oxygen concentration of 10.0% 45min. 2, the method of administration and dose: after artery ligation and hypoxia were instantly via intraperitoneal injection of the the edaravone injection (10mg/kg) or the same volume of saline as control. Pathological examination of brain tissue: HI 3h, 24h, 72h after reperfusion remove brain tissue fixed after conventional dehydration, embedding, serial sections of microtubule-associated protein 2 (microtubule-associated protein 2, MAP2), denitrification -tyrosine (Nitrotysine), 4 - hydroxy nonenal (4-HNE) expression was detected. 4. Half caspase 3 and fodrin determination HI: 6 HI after 24h Wt mice and Hq mice control group, treatment group, respectively, to take the bilateral cerebral hemispheres homogenate fluorescence spectroscopic spectrophotometric determination of half caspase-3 activity; immunoblotting Determination fodrin protein content observed calpain and caspase enzyme 3 activity. Half caspases -3 Edaravone treatment nitrotyrosine determination: 5 Wt mice of the control group and the treatment group the Hq mice of the control group and the treatment group seven, HI 24h after The mice were decapitated, and the left and right hemispheres of the brain ultrasonic homogenizer, using fluorescence spectrophotometry 3 activity of caspase enzymes, protein blotting assay nitrotyrosine content. 6 Statistical analysis: values ??mean ± standard deviation ((?) ± s) said, using the Students t-test method for testing the StatView 5.0 software. P <0.05 was considered statistically significant. Results 1. The cerebral cortex, hippocampus, striatum, and thalamus were seen after HI infarct. Hq brain damage in mice than Wt mice reduced. 2. Male Hq the mouse infarct volume (6.55 ± 0.99mm ~ 3) 52.6% less than male Wt mice infarction volume (13.82 ± 1.86mm ~ 3). 3. Hq mice with Wt mice organizations in HI brain fodrin immunoblotting half caspases -3, no significant difference in the activation of the calcium-dependent protease. 4. Hq mice after HI the 3h-nitrotyrosine positive cells was significantly higher than Wt mice (P <0.05). 5. Edaravone treatment can significantly reduce the formation of the Hq mice nitrotyrosine and lipid peroxidation. 6. Edaravone had no significant effect on caspase activity of. Conclusion The low levels of AIF expression neuroprotective effect on the immature brain hypoxic-ischemic brain injury; Edaravone can enhance this protective effect.

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