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Graphene oxide enhances β-amyloid clearance by inducing autophagy of microglia and neurons.
Chemico-Biological Interactions ( IF 4.7 ) Pub Date : 2020-05-11 , DOI: 10.1016/j.cbi.2020.109126 Xiaolin Li 1 , Kai Li 1 , Fangxuan Chu 1 , Jie Huang 2 , Zhuo Yang 1
Chemico-Biological Interactions ( IF 4.7 ) Pub Date : 2020-05-11 , DOI: 10.1016/j.cbi.2020.109126 Xiaolin Li 1 , Kai Li 1 , Fangxuan Chu 1 , Jie Huang 2 , Zhuo Yang 1
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Alzheimer's disease (AD) is a common neurodegenerative disease, and its pathogenesis is closely related to β-amyloid (Aβ) peptide. The deposition of Aβ in the brain due to impaired Aβ clearance is considered as an important cause of AD. The decrease in Aβ clearance is closely related to the autophagy dysfunction in brains of AD patients. It is feasible to treat AD by increasing the autophagy level of cells such as microglia and neurons to accelerate Aβ clearance. In this article we explored the ability of graphene oxide (GO) to clear Aβ through activating autophagy. Our work demonstrated that GO could inhibit the mTOR signaling pathway by activating AMPK to induce the autophagy of microglial and neurons. As expected, with the improvement of autophagy ability of microglia, GO promoted microglia-mediated Aβ phagocytosis. Under the conditions of co-culture of microglia and neurons, GO induced the autophagy of microglia and neurons, especially the autophagy of microglia, thereby promoting the clearance of Aβ, and ultimately achieved the effect of protecting neurons. Moreover, GO was not only non-cytotoxic to microglia and neurons but also able to reduce the toxicity of Aβ to neurons through its clearance. These results have shown the potential of GO in treating Alzheimer's disease.
中文翻译：
氧化石墨烯通过诱导小胶质细胞和神经元自噬来增强β-淀粉样蛋白的清除。
阿尔茨海默氏病（AD）是一种常见的神经退行性疾病，其发病机理与β-淀粉样蛋白（Aβ）肽密切相关。由于Aβ清除能力受损而导致的Aβ在脑中的沉积被认为是AD的重要原因。Aβ清除率的降低与AD患者大脑中的自噬功能障碍密切相关。通过增加细胞（例如小胶质细胞和神经元）的自噬水平以加速Aβ清除来治疗AD是可行的。在本文中，我们探讨了氧化石墨烯（GO）通过激活自噬清除Aβ的能力。我们的工作表明GO可以通过激活AMPK诱导小胶质细胞和神经元自噬来抑制mTOR信号通路。不出所料，随着小胶质细胞自噬能力的提高，GO促进了小胶质细胞介导的Aβ吞噬作用。在小胶质细胞与神经元共培养的条件下，GO诱导了小胶质细胞与神经元的自噬，特别是小胶质细胞的自噬，从而促进了Aβ的清除，最终达到了保护神经元的作用。此外，GO不仅对小胶质细胞和神经元无细胞毒性，而且还能够通过其清除减少Aβ对神经元的毒性。这些结果显示了GO在治疗阿尔茨海默氏病中的潜力。
更新日期：2020-05-11
中文翻译：
氧化石墨烯通过诱导小胶质细胞和神经元自噬来增强β-淀粉样蛋白的清除。
阿尔茨海默氏病（AD）是一种常见的神经退行性疾病，其发病机理与β-淀粉样蛋白（Aβ）肽密切相关。由于Aβ清除能力受损而导致的Aβ在脑中的沉积被认为是AD的重要原因。Aβ清除率的降低与AD患者大脑中的自噬功能障碍密切相关。通过增加细胞（例如小胶质细胞和神经元）的自噬水平以加速Aβ清除来治疗AD是可行的。在本文中，我们探讨了氧化石墨烯（GO）通过激活自噬清除Aβ的能力。我们的工作表明GO可以通过激活AMPK诱导小胶质细胞和神经元自噬来抑制mTOR信号通路。不出所料，随着小胶质细胞自噬能力的提高，GO促进了小胶质细胞介导的Aβ吞噬作用。在小胶质细胞与神经元共培养的条件下，GO诱导了小胶质细胞与神经元的自噬，特别是小胶质细胞的自噬，从而促进了Aβ的清除，最终达到了保护神经元的作用。此外，GO不仅对小胶质细胞和神经元无细胞毒性，而且还能够通过其清除减少Aβ对神经元的毒性。这些结果显示了GO在治疗阿尔茨海默氏病中的潜力。
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