{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T00:01:37Z","timestamp":1787788897870,"version":"build-2784847793"},"reference-count":63,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,8,5]],"date-time":"2021-08-05T00:00:00Z","timestamp":1628121600000},"content-version":"vor","delay-in-days":216,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31872518"],"award-info":[{"award-number":["31872518"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>Aspirin eugenol ester (AEE) is a new pharmaceutical compound esterified by aspirin and eugenol, which has anti\u2010inflammatory, antioxidant, and other pharmacological activities. The aim of this study was to investigate the protective effect of AEE on paraquat\u2010 (PQ\u2010) induced cell damage of SH\u2010SY5Y 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\u2010dependent manner. However, AEE reduced the PQ\u2010induced loss of cell viability. Flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and 4\u2009<jats:sup>\u2032<\/jats:sup>6\u2010diamidino\u20102\u2010phenylindole (DAPI) staining were used to evaluate cell apoptosis. Compared with the PQ group, AEE pretreatment could significantly inhibit PQ\u2010induced cell damage. AEE pretreatment could reduce the cell damage of SH\u2010SY5Y 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 (<jats:italic>\u0394<\/jats:italic><jats:italic>\u03a8<\/jats:italic><jats:italic>m<\/jats:italic>). At the same time, AEE could increase the activity of glutathione peroxidase (GSH\u2010Px), 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\u2010PI3K, p\u2010Akt, and Bcl\u20102 was significantly decreased, while the expression of caspase\u20103 and Bax was significantly increased in the PQ group. In the AEE group, AEE pretreatment could upregulate the expression of p\u2010PI3K, p\u2010Akt, and Bcl\u20102 and downregulate the expression of caspase\u20103 and Bax in SH\u2010SY5Y cells. PI3K inhibitor LY294002 and the silencing of PI3K by shRNA could weaken the protective effect of AEE on PQ\u2010induced SH\u2010SY5Y cells. Therefore, AEE has a protective effect on PQ\u2010induced SH\u2010SY5Y cells by regulating the PI3K\/Akt signal pathway to inhibit oxidative stress.<\/jats:p>","DOI":"10.1155\/2021\/6697872","type":"journal-article","created":{"date-parts":[[2021,8,6]],"date-time":"2021-08-06T06:37:45Z","timestamp":1628231865000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Protective Activity of Aspirin Eugenol Ester on Paraquat\u2010Induced Cell Damage in SH\u2010SY5Y 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