期刊文献+

缺血/再灌注不同时间点大鼠海马基质细胞诱导因子1α和趋化因子受体4的表达变化

Expressional changes of stromal cell-derived factor 1α and C-X-C chemokine receptor type 4 protein in the hippocampus of ischemia/reperfusion rat
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摘要 目的:研究脑缺血损伤后大鼠海马基质细胞诱导因子1α(SDF-1α)和CXCR4蛋白的表达变化情况。方法:运用免疫组织化学和免疫印迹检测SDF-1α和CXCR4的表达变化。结果:免疫组织化学显色显示,大鼠海马CA区和DG区均可见SDF-1α和CXCR4表达阳性的细胞,其胞质呈棕黄色,DG区主要表达于齿状回颗粒细胞下层。表达SDF-1α和CXCR4的阳性细胞数均随时间推移而增多。免疫印迹检测进一步表明,脑缺血/再灌后1、3、7d和1个月均可见SDF-1α及CXCR4蛋白表达条带,且SDF-1α的表达随时间而增高,与1d比较,复灌7d、1个月时表达差异有统计学意义;CXCR4蛋白表达也随复灌时间延长而增加,但各组之间的表达无差异。结论:缺血/再灌脑损伤后SDF-1α蛋白表达具有时间差异性,提示SDF-1α在缺血性脑损伤过程中可生成、释放,其与缺血性脑损伤之间存在一定的关系。 Objective: To investigate expression changes of stromal cell-derived factor 1α (SDF-1α) and C X-C chemokine receptor type 4 (CXCR4) proteins in the hippocampus of the ischemia/reperfusion model of rats. Methods: Immunohis tochemistry and Western blotting analyses were used to detect SDF-1 α and CXCR4 expression in the hippocampus of is ehemia/reperfusion rats. Results: Immunohistochemistry showed that the SDF-1 α and CXCR4 were expressed in the CA and DG fields of the hippoeampus, in which cytoplasm was stained, and majority of the positive ceils was expressed in the subgranular zone. The positive cell number of SDF-1α and CXCR4 was increased with extending of time. Western blotting results showed that the protein of SDF-1α and CXCR4 was expressed in the hippocampus at different ischemic/ reperfusion time. The protein expressions of SDF-1α and CXCR4 were increased gradually with time and there was sta tistically significant compared with 1 day in the protein expression of SDF-1α. Conclusion: The SDF 1α expression is temporal different in the hippocampus of ischemic/reperfusion rats. This implies that the SDF-1α can be produced and re- leased during ischemic/reperfusion injury and may be associated with brain ischemic injury.
出处 《解剖学杂志》 CAS CSCD 北大核心 2012年第6期792-795,共4页 Chinese Journal of Anatomy
基金 国家自然科学基金(81171141) 徐州医学院院长专项人才基金(2010KJZ19)
关键词 基质细胞诱导因子1α 趋化因子受体4 缺血 再灌注 海马 stromal cell-derived factor 1α C-X-C chemokine receptor type 4 cerebral ischemia/reperfusion hippocampus
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