p38MAPK在大鼠脊髓损伤后胶质瘢痕形成早期对GFAP、vimentin表达的调控作用

基础医学与临床 ›› 2016, Vol. 36 ›› Issue (4): 462-467.

p38MAPK在大鼠脊髓损伤后胶质瘢痕形成早期对GFAP、vimentin表达的调控作用

王富贵¹,夏永智¹,余海军²,马岚²,刘敬贤¹,晏怡¹

1. 重庆医科大学附属第一医院
2. 重庆医科大学

收稿日期:2015-10-13 修回日期:2016-01-03 出版日期:2016-04-05 发布日期:2016-03-29
通讯作者: 晏怡 E-mail:yanyi2005@vip.sina.com
基金资助:
ASK1信号通路在大鼠脊髓损伤后炎症诱导胶质瘢痕形成中的作用及机（国家自然科学基金资助项目）;PAR2参与脊髓损伤后炎症诱导胶质瘢痕形成的机制及亚低温的干预作用（重庆市自然科学基金资助项目）;国家临床重点专科建设经费

The regulation of p38MAPK on GFAP and vimentin expressions at the early stage of glia scar formation after spinal cord injury in rats

Received:2015-10-13 Revised:2016-01-03 Online:2016-04-05 Published:2016-03-29

摘要/Abstract

摘要： 目的探讨在大鼠脊髓损伤（SCI）后胶质瘢痕形成早期，p38丝裂原活化蛋白激酶（p38MAPK）对神经胶质纤维酸性蛋白（GFAP）及波形蛋白(vimentin)表达的影响。方法将大鼠随机分为假手术组（sham group）、模型组（model group）、p38MAPK特异性激动剂anisomycin组（anisomycin group）和p38MAPK特异性抑制剂SB203580组（SB203580 group）。脊髓夹伤模型制作成功后即分别在损伤区硬脊膜下注射生理盐水、anisomycin和SB203580各10 ?L，假手术组只打开椎板暴露脊髓，不做其他处理。于术后第1、3、7及14 d利用BBB评分评定大鼠后肢运动功能，用Western blot和免疫荧光标记技术检测GFAP和vimentin表达。结果术后第14 d，模型组BBB评分显著低于假手术组（p<0.01）；SB203580组大鼠BBB评分显著高于模型组（p<0.05）但仍低于假手术组（p<0.01），而anisomycin组则显著低于模型组（p<0.05）。术后第7和14 d，模型组GFAP、vimentin的表达显著高于假手术组（p<0.01）；SB203580组GFAP、vimentin的表达均显著低于模型组（p<0.05）但仍高于假手术组（p<0.05），而anisomycin组GFAP、vimentin的表达均显著高于模型组（p<0.05）。结论 SCI后胶质瘢痕形成早期p38MAPK可调控GFAP、vimentin的表达，抑制p38MAPK可降低GFAP、vimentin的表达，减轻大鼠SCI后胶质瘢痕形成，促进神经功能的恢复。

关键词: 脊髓损伤, p38丝裂原活化蛋白激酶, GFAP, vimentin

Abstract: Objective To explore p38 mitogen-activated protein kinase(p38MAPK) regulating glial fibrillary acidic protein(GFAP) and vimentin expressions at the early stage of glia scar formation after spinal cord injury in rats. Methods Rats were divided into sham group, model group, p38MAPK specific agonists group(anisomycin group) and p38MAPK specific inhibitor group(SB203580 group) randomly. Normal saline(model group), p38MAPK agonist anisomycin(anisomycin group), p38MAPK inhibitor SB203580(SB203580 group) every 10 ?L were respectively injected in the damaged area under spinal dura mater after the experimental model of SCI were created by extradural compression of the spinal cord using an aneurysm clip, and the sham group rats underwent laminectomy without SCI. The hind legs movement function of rats was evaluated by BBB scale on the 1st, 3rd, 7th and 14th day after SCI, and the the expressions of GFAP and vimentin were detected by western blotting and immunofluorescence assay. Results On the 14th day after SCI, the BBB scores of model group was significantly lower than that of sham group(p<0.01). the BBB scores of SB203580 group was significantly higher than that of model group(p<0.05), but was still lower than that of sham group(p<0.01), and the BBB scores of anisomycin group was significantly lower than that of model group(p<0.05). On the 7th and 14th day after SCI, the expressions of GFAP and vimentin in the model group was significantly higher than that in sham group(p<0.01). the expressions of GFAP and vimentin in SB203580 group was significantly lower than that in model group(p<0.05), but was still higher than that in sham group(p<0.05), and the expresssions of GFAP and vimentin in anisomycin group was significantly higher than that in model group(p<0.05). Conclusion p38MAPK can regulate the expressions of GFAP and vimentin at the early stage of glial scar formation after SCI. Inhibit p38MAPK can reduce the expressions of GFAP and vimentin, lighten glial scar formation after SCI in rats, promote the recovery of neural function.

Key words: spinal cord injury, p38 mitogen-activated protein kinase, GFAP, vimentin

中图分类号:

R651

王富贵夏永智余海军马岚刘敬贤晏怡. p38MAPK在大鼠脊髓损伤后胶质瘢痕形成早期对GFAP、vimentin表达的调控作用[J]. 基础医学与临床, 2016, 36(4): 462-467.

[1]	姚景宏, 李加欢, 刘子建. TLR3激活协同干扰素α抑制小鼠海马神经元DISC1表达[J]. 基础医学与临床, 2022, 42(12): 1855-1860.
[2]	赵方毓, 覃晓莉, 何一多, 王凤杰, 唐鲜娥, 彭新鑫, 陈显兵. 蛇菰多糖减轻急性脊髓挫伤模型大鼠的神经元损伤[J]. 基础医学与临床, 2022, 42(10): 1509-1513.
[3]	陈胜, 王春明, 严雪飞, 毛渊青. 特异性坏死性凋亡抑制剂-1(Nec-1)减轻脊髓损伤模型大鼠胶质瘢痕的形成[J]. 基础医学与临床, 2022, 42(1): 94-99.
[4]	贾春松, 赵彦坡, 尚振华, 邢添瑛, 欧彤文. RNA干扰降低膀胱TGF-β1表达能够改善脊髓损伤大鼠的膀胱功能和纤维化[J]. 基础医学与临床, 2021, 41(7): 1007-1012.
[5]	曾茜, 詹琪, 高远, 崔乃浩, 冯鲁乾. 电刺激促进大鼠脊髓钝挫伤后运动功能恢复[J]. 基础医学与临床, 2020, 40(3): 363-367.
[6]	刘敬贤夏永智王富贵唐维晏怡. IL-1β通过JAK2-STAT3促进大鼠脊髓损伤后胶质瘢痕形成[J]. 基础医学与临床, 2017, 37(5): 668-675.
[7]	陈叶王曼伊胡婷婷黄爽冯乔王平冯乐平. 调控Nampt对DN肾小球细胞表达vimentin的影响[J]. 基础医学与临床, 2016, 36(11): 1505-1510.
[8]	孔令胜聂冬丽张军臣张浩许华. 移植胚鼠神经干细胞对大鼠脊髓损伤后红核神经元损伤作用的影响[J]. 基础医学与临床, 2010, 30(4): 394-397.
[9]	王丽晖吴广礼张丽霞黄旭东李赛. 缬沙坦抑制高糖培养的大鼠肾小球系膜细胞细胞外基质及CTGF的表达[J]. 基础医学与临床, 2009, 29(8): 821-826.