小胶质细胞
罗格列酮
神经毒性
促炎细胞因子
一氧化氮
肿瘤坏死因子α
p38丝裂原活化蛋白激酶
化学
神经炎症
细胞生物学
药理学
磷酸化
蛋白激酶A
炎症
受体
生物
内分泌学
医学
免疫学
内科学
生物化学
毒性
作者
Xiuquan He,Lei Feng,Haiwei Meng,Xiaohong Wang,Shuwei Liu
标识
DOI:10.3109/00207454.2012.686544
摘要
Recent evidence has suggested that microglia activation plays an important role in the pathogenesis of Parkinson's disease (PD). Activated microglia secrete various proinflammatory cytokines and neurotoxic mediators, which may contribute to the development of PD. Thus, the inhibition of microglia activation may have a therapeutic benefit in the treatment of PD. In the present study, using mesencephalic neuron-microglia mixed culture and microglia-enriched culture, we investigated whether rosiglitazone (RGZ), a member of peroxisome proliferator-activated receptor gamma (PPARγ) agonists, could inhibit microglia activation. Our results showed that RGZ significantly inhibited lipopolysaccharide (LPS)-induced microglia activation and the production of tumor necrosis factor-alpha (TNF-α), nitric oxide (NO), and superoxide. We further investigated the intracellular signaling pathways regulating the production of TNF-α and NO in LPS-activated microglia. The results showed that RGZ inhibited the phosphorylation and nuclear translocation of the p65 subunit of NF-κB, and the phosphorylation of p38 mitogen-activated protein kinase (p38MAPK). Taken together, our results suggested that the therapeutic effects of RGZ were partially mediated by modulating microglia activation.
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