Objective To study the neuroprotective mechanism of minocycline against vascular cognitive impairment after cerebral ischemia. Methods The rat model with vascular cognitive impairment was established by permanent bila...
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Objective To study the neuroprotective mechanism of minocycline against vascular cognitive impairment after cerebral ischemia. Methods The rat model with vascular cognitive impairment was established by permanent bilateral common carotid artery occlusion （BCCAO）. The observing time-points were determined at 4, 8 and 16 weeks after BCCAO. Animals were randomly divided into sham-operated group （n = 6）, model group （subdivided into 3 groups： 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6）, and minocycline group （subdivided into 3 groups： 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6）. Minocycline was administered by douche via stomach after BCCAO until sacrifice. Glial fibrillary acidic protein （GFAP） was examined by Western blotting and immunohistochemistry. Levels of cyclooxygenase-2 （COX-2） and nuclear factor-kappaB （NF-κB） were measured by immunohistochemistry. IL-1β and TNF-α levels were tested with ELISA method. Results Levels of GFAP, COX- 2, NF-κB, IL-1β and TNF-α were all up-regulated after permanent BCCAO, which could be significantly inhibited by minocycline. Conclusion Minocycline could ameliorate the inflammation and oxidative stress in the hippocampus of the vascular cognitive impairment rat model.
目的研究慢性铅暴露对原代培养的大鼠脑星形胶质细胞增殖、形态、细胞周期以及葡萄糖调节蛋白78(glucose regulated proteins,GRP78)、生长抑制DNA损伤诱导因子(growth arrest and DNA damage inducible gene,GADD153)和细胞周期蛋白D1(...
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目的研究慢性铅暴露对原代培养的大鼠脑星形胶质细胞增殖、形态、细胞周期以及葡萄糖调节蛋白78(glucose regulated proteins,GRP78)、生长抑制DNA损伤诱导因子(growth arrest and DNA damage inducible gene,GADD153)和细胞周期蛋白D1(CyclinD1)表达的影响,探讨脑星形胶质细胞中铅所诱导的内质网应激反应。方法出生1～4d Wistar大鼠脑星形胶质细胞原代培养并传代,分为对照组和染毒组。分别应用四甲基偶氮唑蓝(methyl thiazolyl tetrazolium,MTT)、流式细胞术、倒置显微镜观察1.0μmol/L乙酸铅染毒细胞增殖率、细胞周期和形态的变化。利用Western blotting检测乙酸铅对星形胶质细胞GRP78、GADD153和CylcinD1表达的影响。结果染铅30d后细胞增殖率下降50.8%。染铅8、12、15和30d后,停留在G1期的细胞数由(58.64±1.75)%分别增加至(69.81±1.56)%、(70.80±1.27)%、(90.59±1.25)%和(80.9±1.11%)。1.0μmol/L乙酸铅呈时间依赖性促进GRP78表达,抑制CyclinD1表达,差异有统计学意义(P<0.05),而GADD153的表达无显著性改变。结论铅可使原代培养的大鼠脑星形胶质细胞发生增殖抑制、细胞周期停滞、GRP78表达上调、CyclinD1表达下调等一系列应激反应。
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