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Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?

机译:甲基厚朴酚可减轻神经炎症:大麻素受体的作用?

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The cannabinoid type-2 G protein-coupled (CB2) receptor is an emerging therapeutic target for pain management and immune system modulation. In a mouse model of Alzheimer’s disease (AD) the orally administered natural product 4′-O-methylhonokiol (MH) has been shown to prevent amyloidogenesis and progression of AD by inhibiting neuroinflammation. In this commentary we discuss an intriguing link between the recently found CB2 receptor-mediated molecular mechanisms of MH and its anti-inflammatory and protective effects in AD animal models. We argue that the novel cannabimimetic MH may exert its beneficial effects via modulation of CB2 receptors expressed in microglial cells and astrocytes. The recent findings provide further evidence for a potential role of CB2 receptors in the pathophysiology of AD, spurring target validation and drug discovery.
机译:大麻素2 G型蛋白偶联(CB2)受体是疼痛控制和免疫系统调节的新兴治疗靶标。在阿尔茨海默氏病(AD)的小鼠模型中,口服天然产物4'-O-甲基厚朴酚(MH)已显示可通过抑制神经炎症来预防淀粉样蛋白生成和AD的进展。在这篇评论中,我们讨论了最近发现的CB2受体介导的MH分子机制与其在AD动物模型中的抗炎和保护作用之间的有趣联系。我们认为,新型大麻拟南芥可能通过调节在小胶质细胞和星形胶质细胞中表达的CB2受体发挥其有益作用。最近的发现为CB2受体在AD的病理生理中的潜在作用提供了进一步的证据,从而促进了靶标的验证和药物的发现。

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