蝎毒耐热合成肽通过 TLR4 介导的自噬激活 PI3K/AKT/NF-κB 信号通路对 PM 诱导的小胶质细胞极化的保护作用。
Protective effect of scorpion venom heat-resistant synthetic peptide against PM-induced microglial polarization via TLR4-mediated autophagy activating PI3K/AKT/NF-κB signaling pathway.
机构信息
College of Medical Laboratory, Dalian Medical University, Dalian 116044, Liaoning Province, China.
College of Medical Laboratory, Dalian Medical University, Dalian 116044, Liaoning Province, China; National-Local Joint Engineering Research Center for Drug-Research and Development (R & D) of Neurodegenerative Diseases, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
出版信息
J Neuroimmunol. 2021 Jun 15;355:577567. doi: 10.1016/j.jneuroim.2021.577567. Epub 2021 Apr 2.
There is growing evidence that fine particulate matter (PM) is a considerable risk factor for neurodegenerative diseases. Scorpion venom heat-resistant synthetic peptide (SVHRSP) plays a neuroprotective effect by promoting neurogenesis and neuron axon growth. In this study, SVHRSP inhibited the level of TLR4, autophagy and PM2.5-induced microglia M1 polarization, thereby promoting Phosphorylation of PI3K and AKT, inhibiting the expression of NF-κB. Moreover, SVHRSP suppressed the cytotoxic factors and increased the cytoprotective factor. This research demonstrates that SVHRSP relieves PM-induced microglial polarization via TLR4-mediated autophagy activating PI3K/AKT/NF-κB signaling pathway, which provides new insights for the treatment of PM-induced neurodegenerative diseases.
越来越多的证据表明，细颗粒物（PM）是神经退行性疾病的一个相当大的风险因素。蝎毒液耐热合成肽（SVHRSP）通过促进神经发生和神经元轴突生长发挥神经保护作用。在这项研究中，SVHRSP 抑制 TLR4、自噬和 PM2.5 诱导的小胶质细胞 M1 极化的水平，从而促进 PI3K 和 AKT 的磷酸化，抑制 NF-κB 的表达。此外，SVHRSP 抑制细胞毒性因子并增加细胞保护因子。这项研究表明，SVHRSP 通过 TLR4 介导的自噬激活 PI3K/AKT/NF-κB 信号通路缓解 PM 诱导的小胶质细胞极化，为治疗 PM 诱导的神经退行性疾病提供了新的思路。
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