Amyloid beta is a major constituent of the plaques found in the brains of patients suffering from Alzheimer's disease (AD). A growing body of research work suggests that neuroinflammation plays important roles in the development of AD. Thus, considerable efforts are directed towards identification of compounds that can reduce or inhibit neuroinflammation. Here, we show that sinomenine, a compound present in a Chinese medicinal plant, Sinomenium acutum, inhibits oligomeric amyloid beta-induced production of reactive oxygen species (ROS), nitric oxide (NO) and inflammation-related molecules from astrocytic cells. The conditioned medium from oligomeric amyloid beta-treated astrocytic cells induces cell death in the hippocampal neuronal cells. Importantly, sinomenine inhibits this cell death. In addition, this compound has inhibitory effects on the production of ROS, NO and inflammation-related factors from oligomeric amyloid-beta treated human astrocytes. Finally, the conditioned medium from oligomeric amyloid beta-treated human astrocytes induces cell death in the primary culture of human neurons, which is inhibited by sinomenine. Thus, sinomenine inhibits amyloid beta-induced production of toxic factors from astrocytes, and confers protection to hippocampal neuronal cells as well as human neurons against indirect toxicity. The results suggest that this compound could provide beneficial effects in AD and other neurodegenerative conditions by reducing inflammation and neuronal cell death.

中文翻译：

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青藤碱抑制淀粉样β诱导的星形胶质细胞活化，并保护神经元免受间接毒性。

β淀粉样蛋白是罹患阿尔茨海默氏病（AD）的患者大脑中斑块的主要成分。越来越多的研究工作表明，神经炎症在AD的发展中起着重要的作用。因此，相当大的努力致力于鉴定可以减少或抑制神经炎症的化合物。在这里，我们显示青藤碱（一种存在于中药材中的化合物）可以抑制寡聚淀粉样β诱导的星形胶质细胞产生的活性氧（ROS），一氧化氮（NO）和炎症相关分子的产生。来自寡聚淀粉样蛋白β处理的星形细胞的条件培养基诱导海马神经元细胞死亡。重要的是，青藤碱可抑制这种细胞死亡。此外，该化合物对经寡聚淀粉样蛋白β处理的人星形胶质细胞产生ROS，NO和炎症相关因子具有抑制作用。最后，来自经寡聚淀粉样蛋白β处理的人类星形胶质细胞的条件培养基在人类神经元的原代培养物中诱导细胞死亡，这被青藤碱抑制。因此，青藤碱抑制淀粉样蛋白诱导的星形胶质细胞毒性因子的产生，并赋予海马神经元细胞和人类神经元针对间接毒性的保护。结果表明，该化合物可通过减少炎症和神经元细胞死亡，在AD和其他神经退行性疾病中提供有益的作用。寡聚淀粉样蛋白β处理过的人星形胶质细胞的条件培养基会诱导人神经元原代培养物中的细胞死亡，而青藤碱会抑制这种死亡。因此，青藤碱抑制淀粉样蛋白诱导的星形胶质细胞毒性因子的产生，并赋予海马神经元细胞和人类神经元针对间接毒性的保护。结果表明，该化合物可通过减少炎症和神经元细胞死亡，在AD和其他神经退行性疾病中提供有益的作用。寡聚淀粉样蛋白β处理过的人星形胶质细胞的条件培养基会诱导人神经元原代培养物中的细胞死亡，而青藤碱会抑制这种死亡。因此，青藤碱抑制淀粉样蛋白诱导的星形胶质细胞毒性因子的产生，并赋予海马神经元细胞和人类神经元针对间接毒性的保护。结果表明，该化合物可通过减少炎症和神经元细胞死亡，在AD和其他神经退行性疾病中提供有益的作用。