尼古丁对脂多糖诱导的小胶质细胞激活及活化后细胞死亡的影响

发布时间：2019-02-18 10:34

【摘要】：目的观察尼古丁对脂多糖(LPS)诱导的小胶质细胞激活及活化后细胞死亡的影响。方法建立慢性尼古丁暴露的小鼠动物模型,腹腔注射LPS诱导小胶质细胞激活,应用免疫组织化学方法观察皮质、海马、黑质CD-11b阳性小胶质细胞表达的变化;BV2细胞(小鼠小胶质瘤细胞系)传代培养,运用CCK-8试剂盒检测细胞活性,一氧化氮检测试剂盒检测一氧化氮(NO)释放情况,RT-PCR分析诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子(TNF-α)、白细胞介素1(IL-1β)、白细胞介素6(IL-6)、环氧化酶-2(COX-2)、干扰素调节因子1(IRF-1)、Caspase-11mRNA的表达,免疫印迹法分析P-I-κB、Caspase-3的表达变化。结果尼古丁抑制LPS诱导的皮质、海马、黑质CD-11b阳性小胶质细胞的表达;尼古丁抑制LPS刺激引起的BV2细胞的死亡,NO的释放,iNOS、TNF-αI、L-1βI、L-6、COX-2I、RF-1、Caspase-11 mRNA的表达,P-I-κB、Caspase-3蛋白的表达。结论尼古丁可以抑制LPS诱导的小胶质细胞活化及激活诱导的细胞死亡(AICD),对脑内炎症反应具有神经保护作用。
[Abstract]:Objective to observe the effect of nicotine on the activation and cell death of lipopolysaccharide (LPS)-induced microglia. Methods LPS was injected intraperitoneally to induce microglia activation, and the expression of CD-11b positive microglia in cortex, hippocampus and substantia nigra was observed by immunohistochemical method. BV2 cells (mouse glioma cell line) were subcultured. The cell activity was detected by CCK-8 kit, nitric oxide (NO) release was detected by nitric oxide assay kit, and inducible nitric oxide synthase (iNOS),) was analyzed by RT-PCR. The expression of tumor necrosis factor (TNF- 伪), interleukin 1 (IL-1 尾), interleukin 6 (IL-6), cyclooxygenase-2 (COX-2), interferon regulatory factor 1 (IRF-1), and Caspase-11mRNA were detected. The expression of P-I- 魏 B caspase-3 was analyzed by Western blot. Results nicotine inhibited the expression of CD-11b positive microglia in cortex, hippocampus and substantia nigra induced by LPS. Nicotine inhibited the death of BV2 cells induced by LPS, the release of NO, the expression of Caspase-11 mRNA and the expression of P-I- 魏 Bmcaspase-3 protein. Conclusion nicotine can inhibit the activation of microglia induced by LPS and the activation of (AICD), induced cell death.
【作者单位】：中国医科大学基础医学院发育生物学教研室;中国医科大学第一附属医院耳鼻咽喉科;
【分类号】：R363

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