Key Laboratory of New Animal Drug Project of Gansu Province, Key Laboratory of Veterinary Pharmaceutical Development of Ministry of Agriculture and Rural Affairs, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China.
Oxid Med Cell Longev. 2021 Jun 24;2021:5527475. doi: 10.1155/2021/5527475. eCollection 2021.
Aspirin eugenol ester (AEE) is a new pharmaceutical compound esterified by aspirin and eugenol, which has anti-inflammatory, antioxidant, and other pharmacological activities. This study is aimed at identifying the protective effect of AEE against HO-induced apoptosis in rat adrenal pheochromocytoma PC12 cells and the possible mechanisms. The results of cell viability assay showed that AEE could increase the viability of PC12 cells stimulated by HO, while AEE alone had no significant effect on the viability of PC12 cells. Compared with the control group, the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were significantly decreased, and the content of malondialdehyde (MDA) was significantly increased in the HO group. By AEE pretreatment, the level of MDA was reduced and the levels of SOD, CAT, and GSH-Px were increased in HO-stimulated PC12 cells. In addition, AEE could reduce the apoptosis of PC12 cells induced by HO via reducing superoxide anion, intracellular ROS, and mitochondrial ROS (mtROS) and increasing the levels of mitochondrial membrane potential (m). Furthermore, the results of western blotting showed that compared with the control group, the expression of p-PI3K, p-Akt, and Bcl-2 was significantly decreased, while the expression of Caspase-3 and Bax was significantly increased in the HO group. In the AEE group, AEE pretreatment could upregulate the expression of p-PI3K, p-Akt, and Bcl-2 and downregulate the expression of Caspase-3 and Bax in PC12 cells stimulated with HO. The silencing of PI3K with shRNA and its inhibitor-LY294002 could abrogate the protective effect of AEE in PC12 cells. Therefore, AEE has a protective effect on HO-induced PC12 cells by regulating the PI3K/Akt signal pathway to inhibit oxidative stress.
阿司匹林丁香酚酯（AEE）是由阿司匹林和丁香酚酯化而成的新型药物化合物，具有抗炎、抗氧化等多种药理活性。本研究旨在探讨 AEE 对 HO 诱导的大鼠肾上腺嗜铬细胞瘤 PC12 细胞凋亡的保护作用及其可能机制。细胞活力检测结果显示，AEE 可增加 HO 刺激的 PC12 细胞活力，而 AEE 单独对 PC12 细胞活力无显著影响。与对照组相比，HO 组超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-Px）活性显著降低，丙二醛（MDA）含量显著升高。经 AEE 预处理后，HO 刺激的 PC12 细胞中 MDA 水平降低，SOD、CAT 和 GSH-Px 水平升高。此外，AEE 可通过减少超氧阴离子、细胞内 ROS 和线粒体 ROS（mtROS），增加线粒体膜电位（m），降低 HO 诱导的 PC12 细胞凋亡。Western blot 结果显示，与对照组相比，HO 组 p-PI3K、p-Akt 和 Bcl-2 表达显著降低，Caspase-3 和 Bax 表达显著升高。在 AEE 组，AEE 预处理可上调 HO 刺激的 PC12 细胞中 p-PI3K、p-Akt 和 Bcl-2 的表达，下调 Caspase-3 和 Bax 的表达。用 shRNA 沉默 PI3K 及其抑制剂 LY294002 可阻断 AEE 在 PC12 细胞中的保护作用。因此，AEE 通过调节 PI3K/Akt 信号通路抑制氧化应激对 HO 诱导的 PC12 细胞具有保护作用。
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