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首页> 外文期刊>Trends in Ecology & Evolution >Mesoporous silica induces hippocampal neurons cell autophagy through AMPK/mTOR/P70S6K signaling pathway
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Mesoporous silica induces hippocampal neurons cell autophagy through AMPK/mTOR/P70S6K signaling pathway

机译:中孔二氧化硅通过AMPK / MTOR / P70S6K信号通路诱导海马神经元细胞自噬

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摘要

Mesoporous silica is a drug carrier with strong targeting, large loading capacity, and easy modification of its surface while its toxicity draws increasing attention recently. In this study, we evaluated the impact of SBA-15 nanomaterials on hippocampal neurons. We found that SBA-15 induces oxidative damage to hippocampal neurons HT22, which further activates autophagy. Treatment with the mammalian target of rapamycin (mTOR) inhibitor AZD8055, the phosphorylation level of mTOR and P70S6K reduced and increased levels of p-AMPK meaning that the adenosine-activated protein kinase (AMPK)/mTOR/P70S6K pathway is involved in SBA-15 induced autophagy of HT22. These results suggested that mesoporous silica material SBA-15 might affect central nervous cells via oxidative stress activation of the AMPK/mTOR/P70S6K pathway, which provides a theoretical basis for safe administration of such materials in patients.
机译:中孔二氧化硅是一种药物载体,其具有强大的靶向,大量负载能力,并且易于改性其表面,而其毒性最近越来越高兴地受到关注。 在这项研究中,我们评估了SBA-15纳米材料对海马神经元的影响。 我们发现SBA-15对海马神经元HT22引起氧化损伤,进一步激活自噬。 用哺乳动物的哺乳动物抑制剂AZD8055治疗,MTOR和P70S6K的磷酸化水平降低和增加的P-AMPK水平,这意味着腺苷活化的蛋白激酶(AMPK)/ mTOR / P70S6K途径参与SBA-15 诱导HT22的自噬。 这些结果表明,中孔二氧化硅材料SBA-15可能通过AMPK / MTOR / P70S6K途径的氧化应激活化来影响中枢神经细胞,这为安全施用这些材料提供了理论依据。

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