丁基苯猷对老化的小胶质细胞诱导多巴胺能神经元损伤的影响
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Effects of dl-3-n-butylphthalide on the damage of dopaminergic neurons induced by age-associated activated microglia
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    【摘要】 目的 探讨dl-3-丁基苯gk(NBP)衰老的小胶质细胞诱导的帕金森病细胞模型中的保护作用及机制。方 法 采用大鼠小胶质细胞原代培养和PC12细胞株的传代培养法,佛波酯诱导小胶质细胞异常活化,不同剂量的NBP 预处理PC12细胞,然后加入低剂量鱼藤酮以建立与衰老小胶质细胞共育系统,模拟帕金森病体外细胞模型,在倒置显 微镜下观察PC12细胞形态,同时用流式细胞仪检测各组PC12线粒体膜电位及细胞内活性氧监测,Annexin V-PI双染 法监测PC12凋亡。结果 与正常组相比,老化小胶质细胞共育的PC12细胞线粒体膜电位下降,细胞内ROS生成增多 (P<0.01),而0.01〜100μM的NBP均可不同程度地抑制这一变化。结论 NBP通过抑制线粒体通透性、减少氧化应激等机制来降低PC12细胞凋亡,对神经元起保护作用。

    Abstract:

    【Abstract】 Objective To investigated the neuroprotective e££ectes of d 1-3-n-Butylphthalide on the damage of dopaminergic neurons induced by age-associated activated microglia. Methods The primary culture of rat microglia and the subculture of PCI 2 cell line were used. Phorbol ester induced the abnormal activation o£ microglia. Different doses of NBP pretreated PCI 2 cells, and then low doses o£ rotenone were added to establish a co culture system with aging microglia 9 simulating the extracellular cell model o£ Parkinson's disease. The morphology o£ PCI 2 cells was observed under the inverted microscope, and flow cytometry was used. The mitochondrial membrane potential and intracellular reactive oxygen species o£ PCI 2 were detected, and the apoptosis o£ PCI 2 was detected by annexin V PI double staining. Results Compared with the normal group, the mitochondrial membrane potential of PCI2 cells co cultured with aged microglia decreased and ROS production increased (P< 0. 01) , while NBP o£ 0. 01~100 μm could inhibit this change in varying degrees. Conclusion NBP can reduce apoptosis of PCI 2 cells and protect neurons by inhibiting mitochondrial permeability and reducing oxidative stress.

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  • 在线发布日期: 2020-02-13
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