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热休克蛋白60在纳洛酮神经保护中的作用

发布时间:2018-08-05 15:33
【摘要】:目的研究热休克蛋白(HSP)60在纳洛酮神经保护中的作用及机制。方法培养小胶质细胞株BV2,实验分为对照组、阳性对照组(细菌脂多糖,LPS)、实验组(LPS+纳洛酮)。利用Western印迹和免疫荧光技术检测不同分组中HSP60的表达,ELISA技术检测HSP60的胞外释放。利用人重组HSP60(rh HSP60)作用于BV2细胞,然后用Western印迹技术检测不同分组中Toll样受体(TLR)-4的表达;收集细胞培养液,用ELISA检测肿瘤坏死因子(TNF)-α和γ-干扰素(IFN-γ)的水平。结果与对照组相比,阳性对照组中的HSP60和TLR-4表达及TNF-α和IFN-γ的释放都显著增加;而加入纳洛酮后,实验组中这些因子的水平都明显降低(P0.05)。结论纳洛酮可能通过HSP60-TLR-4途径阻止小胶质细胞的活化而发挥神经保护作用。
[Abstract]:Objective to study the role and mechanism of heat shock protein (HSP) 60 (HSP60) in the neuroprotection of naloxone. Methods microglia cell line BV2 was cultured and divided into control group, positive control group (lipopolysaccharide) and LPS naloxone group. The expression of HSP60 in different groups was detected by Western blot and immunofluorescence. The extracellular release of HSP60 was detected by Elisa. Human recombinant HSP60 (rh HSP60) was used to treat BV2 cells, then the expression of Toll like receptor (TLR) 4 was detected by Western blotting, and the levels of (TNF) 伪 and IFN- 纬 were detected by ELISA. Results compared with the control group, the expression of HSP60 and TLR-4 and the release of TNF- 伪 and IFN- 纬 in the positive control group were significantly increased, but the levels of these factors in the experimental group were significantly decreased after the addition of naloxone (P0.05). Conclusion Naloxone may play a neuroprotective role by blocking the activation of microglia through HSP60-TLR-4 pathway.
【作者单位】: 宁夏医科大学宁夏颅脑疾病重点实验室;银川市第一人民医院高压氧科;
【基金】:国家自然科学基金(No.31260243)
【分类号】:R96

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