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作 者:徐燊[1] 刘家传[1] 王春琳[1] 王金标[1] 杨艳艳[1] 刘光杰[1]
机构地区:[1]安徽医科大学附属解放军临床学院 解放军105医院神经外科,合肥230031
出 处:《中国微侵袭神经外科杂志》2015年第11期510-513,共4页Chinese Journal of Minimally Invasive Neurosurgery
基 金:全军医学科技"十二五"科研面上项目(编号:CWS11J262);2009年度南京军区医学科技创新重点课题(编号:09Z009)
摘 要:目的探讨中脑星形胶质细胞源性神经营养因子(MANF)在颅脑损伤大鼠脑皮质表达的变化。方法将108只雄性SD大鼠随机分为实验组(n=96)和对照组(n=12),实验组采用自由落体撞击法构建大鼠创伤性颅脑损伤模型,对照组不做处理。伤后1 h、3 h、6 h、12 h、1 d、3 d、7 d、14 d,采用RT-q PCR、免疫组化染色检测挫伤区周围脑皮质MANF m RNA及蛋白表达变化。结果 MANF m RNA及蛋白的相对表达量在颅脑损伤后1 h即开始升高,6 h达高峰,之后开始下降,14 d时与对照组无差异,1 h^7 d各时间点实验组表达均高于对照组(P<0.05)。免疫组化染色结果提示:MANF蛋白阳性表达定位于胞质,呈棕褐色或棕黄色。结论颅脑损伤后MANF出现阳性表达,且定位于胞质;MANF m RNA及蛋白表达上调可能与颅脑损伤时激活一种内源性神经保护机制有关,MANF可能作为一种内质网应激敏感蛋白参与颅脑损伤后细胞抗凋亡反应。Objective To investigate the dynamic expression changes of mesencephalic astrocyte-derived neurotrophic factor(MANF)in rat brain cortex after traumatic brain injury(TBI). Methods A total of 108 male Sprague Dawley rats were randomly divided into TBI group(n = 96) and control group(n = 12). The traumatic brain injury model was established in rats of TBI group with free-fall impact method and no injury was performed in the control group. The expressions of MANF m RNA and protein in the brain tissues of contusion zone were detected by RT-q PCR and immunohistochemistry 1, 3, 6, 12 h, and 1, 3, 7, 14 d after injury. Results RT-q PCR and immunohistochemical results showed that the expressions of MANF m RNA and protein in the brain cortex increased at 1 h,reached peak at 6 h and then decreased to normal 14 d after injury in TBI group. Compared with control group, the expressions of MANF m RNA and protein were significantly higher from 1 h to 7 d after injury in TBI group( P〈0.05). Immunohistochemical staining results showed that MANF protein localized in the cytoplasm and appeared tan or brown. Conclusions MANF could appear and locate in the cytoplasm after TBI. Increase of MANF m RNA and protein expressions may be related to activation of an endogenous neuroprotective mechanism of the cells after TBI. MANF may participate in the anti-apoptotic cell response as a stress sensitive protein of endoplasmic reticulum after TBI.
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