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机构地区:[1]南阳医专第一附属医院神经外科,南阳473000
出 处:《中国实用神经疾病杂志》2012年第17期9-11,共3页Chinese Journal of Practical Nervous Diseases
摘 要:目的观察大鼠创伤性脑损伤(TBI)后细胞色素C释放及凋亡因子Bcl-XL和Bcl-XS的表达意义。方法采用大鼠自由落体建立脑损伤模型,分别于伤后2h、6h、12h、24h、72h、120h、168h检测大鼠脑挫裂伤侧海马CA2-CA3区细胞色素C染色阳性细胞(免疫组化法),应用Bcl-XL和Bcl-XS原位杂交法检测Bcl-XL和Bcl-XS mRNA表达。结果脑挫裂伤后,海马CA2-CA3区Cyt-C阳性染色的神经细胞出现具有明显时相性,脑损伤后大鼠脑组织内Bcl-XL、Bcl-XS mRNA出现相应改变。结论大鼠脑挫裂伤后海马CA2-CA3区细胞有相应变化并出现细胞凋亡。Objective To investigate the regularity of the release of cytochrome C and the ~expressions ot BcI-XL, BcL-XS mRNA after traumatic brain injury in rats. Methods Based on the Feeney's model, the release of cytochrome C in CA2-CA3 region of hippoeampus areas of the injured brain was measured by immunohistochemistry. Apoptosis was detected by the Bcl-XL and Bcl-XS in situ hybridization method at 2, 6, 12, 24, 48, 72, 120, 168 hours after TBI. Results Using immunohistochem- istry method, cytochrome C positive neurons appeared after 1 hour and reached the peak 6 hours later, while fell back since 12 hours, and almost disappeared 24, 48, 72, 120, 168 hours later in the CA2-CA3 region of the hippocampus after injury. Using BcI-XL and Bel-XS in situ hybridization method, the ratio of BcI-XL/BcI-XS was higher after injury. Conclusion The peak of cytoehrome C release is earlier than the aoptosis after traumatic brain injury, and cytochrome C is only one of steps in apoptotic cell death after traumatic brain injury.
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