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二羥基異黃酮對星狀神經膠細胞的抗發炎作用 • 阿茲海默症是ㄧ種在老年族群中常見到的失智症。病理上的特徵包括有:神經細胞的減少、神經膠細胞上有amyloid-β(Aβ) 產生不正常的堆積,以及神經元內部出現神經纖維纏繞的現象。這些病理表現中,Aβ在阿茲海默症的病程扮演了重要的角色。Aβ堆積的位置通常在神經膠細胞上,神經膠細胞中的星狀神經膠細胞是影響神經元生長的ㄧ個重要細胞,Aβ會直接刺激星狀神經膠細胞產生活化的現象。當星狀神經膠細胞活化的時候,會釋放出一些發炎性物質或生長因子來對抗外來的傷害。但是,如果刺激性傷害不斷的產生,導致星狀神經膠細胞不斷的被活化,大量的發炎性物質作用下,就可能會造成慢性發炎的現象。過量的發炎反應本身也是一種刺激,會造成更多的傷害,以及導致神經退化性疾病的產生。所以,Aβ和發炎反應都是造成阿茲海默症病理表現的重要原因。這篇研究主要是想探討:在受到Aβ和lipopolysaccharide(LPS)的刺激之前,先加入 • 具有抗發炎作用的藥物daidzein,daidzein是否能減少促進發炎的物質產生。結果顯示daidzein可以減少NO的產生以及降低interleukin-1 (IL-1)、interleukin-6 (IL-6) 和tumor necrosis factor-alpha (TNF-α)的mRNA表現,daidzein在正常情形下也可以促進星狀神經膠細胞的生長;在受到Aβ和LPS刺激下,也可以對星狀神經膠細胞產生保護作用。所以根據結果推測,先加入daidzein或許可以改善發炎反應並且延緩阿茲海默症進一步的惡化。
Anti-inflammation Effect of Daidzein in Astroglial Cells • Alzheimer’s disease (AD) is the common cause of dementia in old people. The pathological hallmarks of AD include neuronal loss, deposition of Amyloid-β(Aβ),and presence of neurofibrillary tangles (NFTs). Among these conditions, Aβplaque plays an important role in the process of AD. In AD brain, Aβ plaque is surrounded by astrocytes, important regulators of neuron survival, and can induce astrocyte • activation. Reactive astrocytes express various regulatory molecules, such as cytokines and growth factors to respond to the pathological process. However,overexpression of activated astrocytes can induce chronic inflammation which results in a deleterious injury. Besides, inflammatory responses alone are also an significant part of neuropathology, initiating stimulus and self-propelling mechanisms. So both Aβ and inflammation are critical to the pathogenesis of alzheimer’s disease. The present study is to see whether daidzein, known to have anti-inflammation activity, is able to inhibit the production of proinflammatory mediators by using two stimulants, • Aβand lipopolysaccharide (LPS). The results indicate that daidzein is able to reduce NO production and mRNA expression of IL-1,IL-6 and TNF-α under Aβand LPS • treatments . It can also promote astrocyte proliferation and protect astrocyte from Aβ and LPS damage. These results further increase the possibility that the positive effects of daidzein may ameliorate the process of inflammation and alleviate the risk of AD.