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论文摘要

大鼠颅脑损伤后突触素表达变化研究

The Alterations in Expression of the Synaptophysin in Rat Brain Trauma Injury Model——an Experimental Study

作者:王焱超, 张瑜, 蓝婷等

Author:WANG Yan-chao, ZHANG Yu, LAN Ting. et al

收稿日期:          年卷(期)页码:2016,47(6):852-856

期刊名称:四川大学学报(医学版)

Journal Name:JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCE EDITION)

关键字:颅脑损伤 动物模型 影像学 组织病理学

Key words:Brain trauma injury Animal model Radiology Histopathology

基金项目:

中文摘要

目的 探讨大鼠颅脑损伤后突触素变化规律并探索其与组织学、影像学的动态变化关系。方法 健康3月龄雄性SD大鼠24只,依据突触素检测时间,分为损伤后2周、4周、8周组和对照组共4组,每组6只。其中3个损伤组通过建立大鼠自由落体脑损伤模型,在损伤后24 h、2周、4周和8周时通过CT检查观察其颅脑损伤后脑组织的影像学变化,对照组不作损伤处理。同时检测大鼠颅脑损伤后脑组织形态学及影像学变化,并分别于2周、4周、8周使用免疫荧光法及蛋白免疫印迹实验观察受伤后大鼠脑组织突触素表达变化。结果 大鼠颅脑损伤后,神经功能评分提示实验组大鼠出现明显神经功能障碍,HE染色提示实验组大鼠受伤24 h出现脑细胞水肿、坏死。另外尚可见局部的充血,受伤后2周后出现脑溶解性液化及坏死,而受伤4周及8周后除可见明显组织缺损外,无明显组织学变化。CT检查提示实验组大鼠术后24 h呈现全脑明显的低密度影,此后脑组织低密度灶的区域及程度开始减轻,至受伤后2周低密度影已经明显减退,受伤后4周及8周时脑损伤已经不明显,仅可见骨窗缺损。免疫荧光染色及western blot均提示突触素表达于2周下降,第8周略有上升。结论 成功建立了Feeney大鼠自由落体脑损伤模型。大鼠颅脑损伤后,突触素在受损急性期呈现下降,持续至脑损伤后第8周开始恢复。突触素的表达随时间变化的规律与影像学、组织病理学变化有关。

英文摘要

Objective To study the rat brain trauma injury model and investigate the rules of transformation of expression of synaptophysin and its relationship between histology and radiology alternation after brain trauma injury. Methods 24 SD male rats aged three months were randomly divided into 4 groups, including a control group of 6 rats. The experimental group rats were received operation to build free falling brain trauma injury model. The rat were analyzed at 2, 4, 8 weeks after injury. The experimental group rat were killed after CT scan and functional evaluation, histological changes were measured through HE staining. Synaptophysin were observed by using immunofluorescence method and Western blot. Results After brain injury the functional evaluation of rat showed dysneuria. Edema and necrosis in neurons and local congestion at 24 h after injury, necrosis and solubility liquefaction at 2 weeks after injury, and histological defects at 4 weeks and 8 weeks after injury, were observed in HE staining in experimental group. The significant cerebral low density shadows at 24 h after injury, lightened in 2 weeks after injury, and disappeared at 4 weeks and 8 weeks after injury, left only the bone defects in CT images. Expression of synaptophysin in brain tissue was decreased from 2 weeks after injury and it was mild increased at 8 weeks after injury evaluated by immunofluorescence method and Western blot. Conclusion The functional evaluation, histological and CT scan result indicate that we have built the rat brain trauma injury model successfully. The damage of synapse was correlated with histological and radiological result. The expression of synaptophysin was decreased form acute stage and gradually increased until 8 weeks after injury. This study can be applied as control in research of nerve regeneration after brain trauma injury.

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