Abstract
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 H2O2-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 H2O2, 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 H2O2 group. By AEE pretreatment, the level of MDA was reduced and the levels of SOD, CAT, and GSH-Px were increased in H2O2-stimulated PC12 cells. In addition, AEE could reduce the apoptosis of PC12 cells induced by H2O2 via reducing superoxide anion, intracellular ROS, and mitochondrial ROS (mtROS) and increasing the levels of mitochondrial membrane potential (ΔΨm). 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 H2O2 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 H2O2. 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 H2O2-induced PC12 cells by regulating the PI3K/Akt signal pathway to inhibit oxidative stress.
Highlights
There are growing evidences that oxidative stress is closely related to human neurodegenerative diseases, including Alzheimer’s disease (AD) and Huntington’s disease (HD) [1,2,3,4,5]
The results showed that Aspirin eugenol ester (AEE) could significantly alleviate the mitochondrial dysfunction of PC12 cells via inhibiting intracellular reactive oxygen species (ROS), mitochondrial ROS (mtROS), and superoxide anion levels
These results showed that AEE may have a protective effect on H2O2-induced PC12 cells via the Phosphatidylinositol 3 kinase (PI3Ks)/Akt pathway
Summary
There are growing evidences that oxidative stress is closely related to human neurodegenerative diseases, including Alzheimer’s disease (AD) and Huntington’s disease (HD) [1,2,3,4,5]. Excessive production of reactive oxygen species (ROS) is one of the main causes of oxidative stress [6,7,8,9]. Excessive ROS stimulates cells to cause structural damage and promotes oxidative stress and destroy the redox balance and lead to cell damage and apoptosis [13,14,15]. There are many closely related antioxidant systems in the body. The main role of antioxidant systems is to prevent oxidative damage to the body by removing excess ROS from cells [16,17,18]. ROS-mediated oxidative stress mainly activates the inherent apoptosis pathway by releasing a variety of prodeath factors into the cytoplasm of damaged
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