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Neuroprotection by Walnut-derived Peptides through Autophagy Promotion via Akt/mTOR Signaling Pathway against Oxidative Stress in PC12 Cells.
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2020-02-22 , DOI: 10.1021/acs.jafc.9b08252 Fanrui Zhao 1, 2 , Ji Wang 1, 2 , Hongyan Lu 1, 2 , Li Fang 1, 2 , Hanxiong Qin 1, 2 , Chunlei Liu 1, 2 , Weihong Min 1, 2
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2020-02-22 , DOI: 10.1021/acs.jafc.9b08252 Fanrui Zhao 1, 2 , Ji Wang 1, 2 , Hongyan Lu 1, 2 , Li Fang 1, 2 , Hanxiong Qin 1, 2 , Chunlei Liu 1, 2 , Weihong Min 1, 2
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Natural-derived peptides are effective substances in attenuating oxidative stress. However, their specific mechanisms have not been fully elucidated, especially in peptide-mediated autophagy. In the present study, TWLPLPR, YVLLPSPK, and KVPPLLY, novel peptides from Juglans mandshurica Maxim, prevented ROS production, elevated GSH-Px activity and ATP levels, and ameliorated apoptosis in Aβ25-35 (at concentration of 50 μM for 24 h) induced PC12 cells (P < 0.01). Both western blot and immunofluorescence analysis illustrated that the peptides regulated Akt/mTOR signaling through p-Akt (Ser473) and p-mTOR (S2481) and promoted autophagy by increasing the levels of LC3-II/LC3-I and Beclin-1, while lowering p62 expression (P < 0.01). Autophagy inhibitor (3-methyladenine, 3-MA) and inducer (Rapamycin, RAPA) were combined used to confirm the contribution of peptide-regulated autophagy in anti-oxidative effects. Moreover, the peptides increased the level of LAMP1, LAMP2, and Cathepsin D (P < 0.05) and promoted the fusion with lysosomes to form autolysosomes, accelerating ROS removal. These data suggested that walnut-derived peptides regulated oxidative stress by promoting autophagy in the Aβ25-35-induced PC12 cells.
中文翻译:
核桃衍生肽通过PC12细胞中抗氧化应激的Akt / mTOR信号通路通过自噬促进的神经保护作用。
天然来源的肽是减轻氧化应激的有效物质。但是,它们的具体机制尚未完全阐明,特别是在肽介导的自噬中。在本研究中,来自胡桃Maxim的新型肽TWLPLPR,YVLLPSPK和KVPPLLY阻止了ROS的产生,GSH-Px活性和ATP水平的升高,并改善了Aβ25-35的凋亡(浓度为50μM,持续24 h)。 PC12细胞(P <0.01)。免疫印迹和免疫荧光分析均表明,该肽通过p-Akt(Ser473)和p-mTOR(S2481)调节Akt / mTOR信号传导,并通过增加LC3-II / LC3-I和Beclin-1的水平促进自噬。降低p62表达(P <0.01)。自噬抑制剂(3-甲基腺嘌呤,3-MA)和诱导剂(雷帕霉素,RAPA)组合用于确认肽调节的自噬在抗氧化作用中的作用。此外,这些肽增加了LAMP1,LAMP2和组织蛋白酶D的水平(P <0.05),并促进了与溶酶体的融合形成自溶酶体,从而加速了ROS的去除。这些数据表明,核桃来源的肽通过促进Aβ25-35诱导的PC12细胞中的自噬来调节氧化应激。
更新日期:2020-03-10
中文翻译:
![](https://scdn.x-mol.com/jcss/images/paperTranslation.png)
核桃衍生肽通过PC12细胞中抗氧化应激的Akt / mTOR信号通路通过自噬促进的神经保护作用。
天然来源的肽是减轻氧化应激的有效物质。但是,它们的具体机制尚未完全阐明,特别是在肽介导的自噬中。在本研究中,来自胡桃Maxim的新型肽TWLPLPR,YVLLPSPK和KVPPLLY阻止了ROS的产生,GSH-Px活性和ATP水平的升高,并改善了Aβ25-35的凋亡(浓度为50μM,持续24 h)。 PC12细胞(P <0.01)。免疫印迹和免疫荧光分析均表明,该肽通过p-Akt(Ser473)和p-mTOR(S2481)调节Akt / mTOR信号传导,并通过增加LC3-II / LC3-I和Beclin-1的水平促进自噬。降低p62表达(P <0.01)。自噬抑制剂(3-甲基腺嘌呤,3-MA)和诱导剂(雷帕霉素,RAPA)组合用于确认肽调节的自噬在抗氧化作用中的作用。此外,这些肽增加了LAMP1,LAMP2和组织蛋白酶D的水平(P <0.05),并促进了与溶酶体的融合形成自溶酶体,从而加速了ROS的去除。这些数据表明,核桃来源的肽通过促进Aβ25-35诱导的PC12细胞中的自噬来调节氧化应激。