Secondary damage caused by CD11b+ microglia following diffuse axonal injury in rats

Secondary damage caused by CD11b+ microglia following diffuse axonal injury in rats
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DOI:
10.1097/ta.0b013e318246eaf4
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发表时间:
2012-11
影响因子:
3.4
通讯作者:
Xianxian Jia;B. Cong;Songjun Wang;Liru Dong;Chunling Ma;Yingmin Li
Xianxian Jia;B. Cong;Songjun Wang;Liru Dong;Chunling Ma;Yingmin Li
中科院分区:
医学2区
文献类型:
--
作者:
Xianxian Jia;B. Cong;Songjun Wang;Liru Dong;Chunling Ma;Yingmin Li

文献摘要

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弥漫性轴索损伤(DAI)是人类创伤性脑损伤最常见和最重要的病理特征之一,具有高死亡率和持续性创伤后神经系统后遗症。继发性损伤,如水肿或炎症引起的质量压缩效应,可加剧受损轴突的形态变化。方法在本研究中,通过对Sprague-Dawley大鼠进行中线闭式颅骨撞击诱导DAI。假手术实验大鼠和对照动物分别于0小时、1小时、3小时、6小时、12小时、24小时、72小时、5天、7天后处死。采集脑组织,石蜡包埋脑组织切片(5 m厚),进行苏木精和伊红染色、Bielschowsky银染色、尼索尔体甲酚紫染色、髓鞘Weil染色或TUNEL染色,以验证神经元的变化。免疫细胞化学检测-淀粉样蛋白前体蛋白、CD11b和白细胞介素(IL)-6的表达。结果CD11b/IL-6表达在损伤后6小时较高,在损伤后12小时达到峰值。损伤后24、48小时神经元病理变化更大。结果表明,DAI可诱导损伤后早期小胶质细胞激活表达IL-6。结论:这表明小胶质细胞在至少部分由IL-6介导的脑组织继发性病理改变中起重要作用。
BACKGROUND Diffuse axonal injury (DAI) is one of the most common and important pathologic features of human traumatic brain injury, accounting for high mortality and the development of persistent posttraumatic neurologic sequelae. Secondary damage resulting, e.g., from mass compressive effects through edema or inflammation can exacerbate morphologic changes in injured axons. METHODS In this study, DAI was induced in Sprague-Dawley rats by subjecting the animals to a midline closed-skull strike. Experimental rats and control animals subjected to sham operation were killed at 0 hour, 1 hour, 3 hour, 6 hour, 12 hour, 24 hour, 72 hour, 5 days, or 7 days later. Brains were harvested and paraffin-embedded sections of brain tissue (5 m thick) were processed for hematoxylin and eosin staining, Bielschowsky silver staining, cresyl violet staining of Nissl bodies, Weil staining of myelin sheaths, or TUNEL assay to verify neuronal changes. Immunocytochemistry was used to examine the expression of -amyloid precursor protein, CD11b, and interleukin (IL)-6. RESULTS CD11b/IL-6 expression was higher at 6 hour and peaked at 12 hour after injury. Pathologic changes in neurons were greater at 24 and 48 hour after injury. The results indicate that DAI can induce activation of microglia to express IL-6 in the early stages after injury. CONCLUSIONS This suggests that microglia play an important role in secondary pathologic changes in brain tissue that are mediated, at least in part, by IL-6.