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作 者:李晓文[1] 曾晓锋[2] 康丽[1] 吴德野[1,3] 郭小兵[1] 于建云[2,4] 李坪[1]
机构地区:[1]昆明医科大学人体解剖学与组织胚胎学系,昆明650500 [2]昆明医科大学法医学院,昆明650500 [3]淄博万杰医学院,山东255213 [4]昆明医科大学脑损伤研究室,昆明650500
出 处:《神经解剖学杂志》2014年第1期29-34,共6页Chinese Journal of Neuroanatomy
基 金:国家自然科学基金(31100769;30560041);云南省自然科学基金(2008CD052)
摘 要:目的:观察单纯性脑震荡(pure cerebral concussion,PCC)大鼠前额叶皮质(prefrontal cortex,PC)、颞叶皮质(temporal cortex,TC)和梨状皮质(piriform cortex,Pir)内小胶质细胞(microglia,MG)的反应和时程变化规律,探讨小胶质细胞与脑损伤之间的病理联系。方法:采用自制金属单摆闭合式脑损伤打击装置制备清醒状态下PCC模型,随机分为伤后3 h、12 h、1 d、2 d、3 d、7 d六个损伤组(n=5),另设正常对照组(n=5)。采用OX-42单克隆抗体(MG特异性标记物)进行免疫组织化学和免疫荧光染色,观察PCC组和正常对照组大鼠PC、TC和Pir中OX-42的表达变化。结果:正常对照组大鼠PC、TC和Pir内OX-42免疫阳性产物的表达很弱,OX-42免疫阳性的小胶质细胞的数量少而轮廓不清。损伤后OX-42免疫阳性产物的表达和阳性细胞的数量逐渐增加,3 d时达高峰,7 d后有下降趋势,但仍高于正常组(P<0.05)。结论:PCC损伤早期PC、TC和Pir中MG出现激活的形态学变化,提示MG可能参与了PCC致伤后的病理变化。Objective: To study the response and change of the microglia(MG) in the prefrontal cortex( PC), temporal cortex(TC) and piriform cortex(Pir) after the pure cerebral concussion(PCC) and to explore the relationship between mi- croglia and pathological changes after brain injury. Methods: Under the waking condition, the PCC models of the rats were established by using a metallic pendulum-striker concussive device. The rats were randomly divided into 3 h, 12 h, 1 d, 2 d, 3 d and 7 d(n = 5)groups after PCC injury. One normal group(n =5) was used as the control. The distribution and changes of OX-42 expression in the PC, TC and Pir between the PCC and the control groups were observed by the im- munohistochemical and immunofluorescence histochemical staining. Results: The expression of OX-42-immunoreaetivity was weak and the profile of a small number of the positive cells was unclear in the control group. The expression of OX- 42-immunoreaetivity and the number of the OX-42-imnlunopositive cells increased gradually from 3 h to 3 d in the PC ,TC and Pir after brain injury when compared with the control group, and were strongest at 3 d and showed a downward but still higher than the control group until 7 d( P 〈 0.05 ). Conclusion: That microglia was activated with the changes in mor- phology and number in the PC ,TC and Pir during the early stage of the brain injury suggest that MG may be involved in the pathological changes after PCC.
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