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羟基酪醇通过激活 PI3K/AKT/mTOR-HIF-1 信号减轻低氧介导的 PC12 细胞损伤。

Hydroxytyrosol Alleviated Hypoxia-Mediated PC12 Cell Damage through Activating PI3K/AKT/mTOR-HIF-1 Signaling.

机构信息

Department of Clinical Pharmacy, The 940th Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Lanzhou 730050, China.

Gansu Plateau Pharmaceutical Technology Center, Lanzhou 730050, China.

出版信息

Oxid Med Cell Longev. 2022 Jun 3;2022:8673728. doi: 10.1155/2022/8673728. eCollection 2022.

DOI:10.1155/2022/8673728
PMID:35693707
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9187455/
Abstract

BACKGROUND

Hypoxia exerts pressure on cells and organisms, and this pressure can occur under both pathological and nonpathological conditions. There are many reports confirmed that hydroxytyrosol has good in vitro antioxidant activity, while the research about hydroxytyrosol on hypoxia-mediated cell damage is still unclear.

PURPOSE

The aim of this study was to investigate the effect and mechanism of hydroxytyrosol on hypoxia-mediated cell damage.

METHODS

We studied the effects of hydroxytyrosol on the content of reactive oxygen species, the change of antioxidant enzymes activity of SOD, CAT, and GSH-Px and the content of oxidation products MDA and GSH, and the changes of cell membrane potential and effect on PI3K/AKT/mTOR-HIF-1 signaling pathway under hypoxia-mediated PC12 cell.

RESULTS

PC12 cell treated with hydroxytyrosol abated the cell apoptosis and alleviated the oxidative stress through scavenging of reactive oxygen species, improving the enzyme activity and changing the content of oxidation products and alleviating mitochondria damage. Western blotting confirmed that the mechanism maybe related to the PI3K/AKT/mTOR-HIF-1 signaling pathway. The inhibition experiment confirmed that hydroxytyrosol takes part in the expression of protein PI3K and p-mTOR.

CONCLUSION

Hydroxytyrosol reduced the oxidative stress and resisted the inhibition of PI3K/AKT/mTOR-HIF-1 signaling pathway caused by hypoxia, improved cell apoptosis, and ameliorated the antihypoxia ability of PC12 cells under hypoxia.

摘要

背景

缺氧对细胞和机体施加压力，这种压力既可以在病理条件下也可以在非病理条件下发生。有许多报道证实，羟基酪醇具有良好的体外抗氧化活性，而关于羟基酪醇对缺氧介导的细胞损伤的研究尚不清楚。

目的

本研究旨在探讨羟基酪醇对缺氧介导的细胞损伤的作用及机制。

方法

研究了羟基酪醇对缺氧诱导的 PC12 细胞内活性氧（ROS）含量、抗氧化酶 SOD、CAT 和 GSH-Px 活性变化、氧化产物 MDA 和 GSH 含量变化、细胞膜电位变化及对 PI3K/AKT/mTOR-HIF-1 信号通路的影响。

结果

PC12 细胞用羟基酪醇处理后，通过清除活性氧，提高酶活性，改变氧化产物含量，减轻线粒体损伤，减轻细胞凋亡，减轻氧化应激。Western blot 证实其机制可能与 PI3K/AKT/mTOR-HIF-1 信号通路有关。抑制实验证实，羟基酪醇参与了蛋白 PI3K 和 p-mTOR 的表达。

结论

羟基酪醇减轻了氧化应激，抑制了缺氧引起的 PI3K/AKT/mTOR-HIF-1 信号通路的抑制，改善了缺氧下 PC12 细胞的细胞凋亡，提高了其抗缺氧能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/9187455/bc090abdbe6f/OMCL2022-8673728.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/9187455/5816cdca640d/OMCL2022-8673728.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/9187455/bc090abdbe6f/OMCL2022-8673728.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/9187455/5816cdca640d/OMCL2022-8673728.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf46/9187455/bc090abdbe6f/OMCL2022-8673728.004.jpg

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