雷公藤甲素抑制培养的大鼠小胶质细胞中β淀粉样蛋白1-42诱导的肿瘤坏死因子-α和白细胞介素-1β的产生。
Triptolide inhibits amyloid-beta1-42-induced TNF-alpha and IL-1beta production in cultured rat microglia.
作者信息
Jiao Jian, Xue Bing, Zhang Lei, Gong Yuntao, Li Kairong, Wang Haomin, Jing Liming, Xie Junxia, Wang Xiaomin
机构信息
Neuroscience Research Institute and Department of Neurobiology, Peking University, Key Laboratory for Neuroscience of the Ministry of Education, 38 Xueyuan Road, Beijing 100083, PR China.
出版信息
J Neuroimmunol. 2008 Dec 15;205(1-2):32-6. doi: 10.1016/j.jneuroim.2008.08.006. Epub 2008 Nov 12.
Microglia plays an important role in mediating neuroinflammation in Alzheimer's disease (AD). Intervention in microglia activation may exert a neuroprotective effect. In the present study, we reported that oligomeric Abeta1-42 dramatically increased the level of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta compared to monomeric and fibrillar Abeta1-42 in rat microglial cultures. Pretreatment of the cultures with triptolide, an anti-inflammatory reagent, alleviated the elevation of TNF-alpha and IL-1beta level induced by oligomeric Abeta1-42. Our results showed that oligomeric Abeta played an important role in mediating neuroinflammation and triptolide was able to suppress the production of pro-inflammatory cytokines from microglia.
小胶质细胞在介导阿尔茨海默病（AD）的神经炎症中起重要作用。干预小胶质细胞激活可能会发挥神经保护作用。在本研究中，我们报告与单体和纤维状Aβ1-42相比，寡聚体Aβ1-42在大鼠小胶质细胞培养物中显著提高了肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1β的水平。用抗炎试剂雷公藤内酯醇预处理培养物，可减轻寡聚体Aβ1-42诱导的TNF-α和IL-1β水平升高。我们的结果表明，寡聚体Aβ在介导神经炎症中起重要作用，雷公藤内酯醇能够抑制小胶质细胞促炎细胞因子的产生。
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