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。
目的研究胰蛋白酶原基因(PRSS1)不同的基因型对乙型肝炎病毒表面抗原的反应性。方法将8例携带PRSS1 A121T(c.361 G>A)突变、12例PRSS1基因沉默突变D162D(c.486 C>T)的胰腺炎患者和16例健康体检者的外周血淋巴细胞分别加于乙型肝炎病毒(hepatitis B virus,HBV)衣壳抗原和0.9%生理盐水进行体外培养,在0、12、24、36、48、72 h计数点对不同组别的淋巴细胞进行充池计数并折算成增殖率,同时用流式细胞术检测CD4、CD8的表达情况,并对不同基因型胰腺炎患者的乙型肝炎病毒表面抗体(hepatitis B surface antibody,anti-HBs)水平在病程中变化情况进行统计分析。结果携带PRSS1基因A121T突变的胰腺炎患者的anti-HBs水平在胰腺炎病程中波动较大,而携带沉默突变的胰腺炎患者与健康对照无显著性差异,在外周血淋巴细胞刺激增殖实验中A121T突变的胰腺炎患者对HBV的反应性呈减弱状态,而沉默突变的胰腺炎患者与健康对照无显著性差异,流式细胞术检测显示PRSS1基因A121T突变的胰腺炎患者的CD4/CD8比值降低。结论来自胰蛋白酶原基因不同基因型的淋巴细胞对乙型肝炎病毒表面抗原的反应性不一,胰蛋白酶原基因突变会干扰T淋巴细胞受体对乙型肝炎病毒表面抗原的反应性。
Objective Nitric oxide （NO） was speculated to play an Minocycline, a tetracycline derivative, reduced inflammation important role in the pathophysiology of cerebral ischemia. and protected against cerebral ischemia....
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Objective Nitric oxide （NO） was speculated to play an Minocycline, a tetracycline derivative, reduced inflammation important role in the pathophysiology of cerebral ischemia. and protected against cerebral ischemia. To study the neuroprotection mechanism of minocycline for vascular dementia, the influences of minocycline on expressions of inducible nitric oxide synthase （iNOS） and endothelial nitric oxide synthase （eNOS） were observed in the brains of Wistar rats. Methods The vascular dementia rat model was established by permanent bilateral common carotid arteries occlusion （BCCAO）. Wistar rats were divideded into 3 groups randomly： sham-operation group （S group）, vascular dementia model group （M group）, and minocycline treatment group （MT group）. The behaviour was tested with Morris water maze and open-field task. Expressions of iNOS and eNOS were measured by immunohistochemistry and reverse transcriptase-polymerase chain reaction （RT-PCR）. The optical density value was measured by imaging analysis. Percentage of positive ceils with iNOS and eNOS expression was analyzed with optical microscope. Results Minocycline attenuated cognitive impairment. Inducible NOS was significantly down-regulated in MT group, compared with that in M group （P 〈 0.01）, while eNOS was significantly up-regulated, compared with that in M group （P 〈 0.01）. The expressions of iNOS and eNOS in M and MT groups were higher than those in S group （P 〈 0.01）. Conclusion Minocycline can down-regulate the expression of iNOS and up-regulate the expression of eNOS in vascular dementia, which restrains apoptosis and oxidative stress to protect neural function.
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