Abstract
Aspirin eugenol ester (AEE) is a new pharmaceutical compound esterified by aspirin and eugenol, which has anti-inflammatory, antioxidant, and other pharmacological activities. The aim of this study was to investigate the protective effect of AEE on paraquat- (PQ-) induced cell damage of SH-SY5Y human neuroblastoma cells and its potential molecular mechanism. There was no significant change in cell viability when AEE was used alone. PQ treatment reduced cell viability in a concentration-dependent manner. However, AEE reduced the PQ-induced loss of cell viability. Flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and 4′6-diamidino-2-phenylindole (DAPI) staining were used to evaluate cell apoptosis. Compared with the PQ group, AEE pretreatment could significantly inhibit PQ-induced cell damage. AEE pretreatment could reduce the cell damage of SH-SY5Y cells induced by PQ via reducing superoxide anion, intracellular reactive oxygen species (ROS), and mitochondrial ROS (mtROS) and increasing the levels of mitochondrial membrane potential (ΔΨm). At the same time, AEE could increase the activity of glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD) and decrease the activity of malondialdehyde (MDA). The results 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 PQ 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 SH-SY5Y cells. PI3K inhibitor LY294002 and the silencing of PI3K by shRNA could weaken the protective effect of AEE on PQ-induced SH-SY5Y cells. Therefore, AEE has a protective effect on PQ-induced SH-SY5Y cells by regulating the PI3K/Akt signal pathway to inhibit oxidative stress.
Highlights
Parkinson’s disease (PD) is a typical age-related chronic progressive disease, and it is one of the most common neurodegenerative diseases [1]
When the cells were treated with 250 μM PQ for 24 h, the cell viability decreased significantly compared with the control group (Figure 1(b))
The pathogenesis of PD is mediated by excessive production of reactive oxygen species (ROS), which will eventually lead to the loss of mitochondrial membrane potential, resulting in the activation of caspase cascade [38–41]
Summary
Parkinson’s disease (PD) is a typical age-related chronic progressive disease, and it is one of the most common neurodegenerative diseases [1]. PD primarily results from the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) [2]. PD is associated with motor impairments including bradykinesia, rigidity, resting tremor, and gait disturbance [3]. Studies showed that oxidative stress, impairment of mitochondrial, and apoptotic cascade activation play important roles in the occurrence and development of PD [4, 5]. To other neurodegenerative diseases, PD patients display increased levels of oxidative stress and ROS, decreased mitochondrial membrane potential, and activated caspase cascade [6, 7]
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