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Protective Activity of Aspirin Eugenol Ester on Paraquat-Induced Cell Damage in SH-SY5Y Cells.
- Source :
-
Oxidative medicine and cellular longevity [Oxid Med Cell Longev] 2021 Aug 04; Vol. 2021, pp. 6697872. Date of Electronic Publication: 2021 Aug 04 (Print Publication: 2021). - Publication Year :
- 2021
-
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 (ΔΨ m ). 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.<br />Competing Interests: The authors declare no conflict of interest.<br /> (Copyright © 2021 Zhen-Dong Zhang et al.)
- Subjects :
- Aspirin pharmacology
Cell Line, Tumor
Cell Survival drug effects
Chromones pharmacology
Down-Regulation drug effects
Eugenol pharmacology
Glutathione Peroxidase metabolism
Humans
Malondialdehyde metabolism
Membrane Potential, Mitochondrial drug effects
Morpholines pharmacology
Phosphatidylinositol 3-Kinases chemistry
Phosphatidylinositol 3-Kinases genetics
Phosphatidylinositol 3-Kinases metabolism
Proto-Oncogene Proteins c-akt metabolism
Proto-Oncogene Proteins c-bcl-2 genetics
Proto-Oncogene Proteins c-bcl-2 metabolism
RNA Interference
RNA, Small Interfering metabolism
Reactive Oxygen Species metabolism
Signal Transduction drug effects
Apoptosis drug effects
Aspirin analogs & derivatives
Eugenol analogs & derivatives
Paraquat toxicity
Protective Agents pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1942-0994
- Volume :
- 2021
- Database :
- MEDLINE
- Journal :
- Oxidative medicine and cellular longevity
- Publication Type :
- Academic Journal
- Accession number :
- 34394831
- Full Text :
- https://doi.org/10.1155/2021/6697872