{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T21:41:41Z","timestamp":1788385301236,"version":"build-2803163510"},"reference-count":37,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2022,7,31]],"date-time":"2022-07-31T00:00:00Z","timestamp":1659225600000},"content-version":"vor","delay-in-days":0,"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":["81871008"],"award-info":[{"award-number":["81871008"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p>Epileptic seizures or status epilepticus (SE) can cause hippocampal neuronal death, which has detrimental effects. Parthanatos, a new form of programmed cell death, is characterized by hyperactivation of poly (ADP\u2010ribose) polymerase\u20101 (PARP\u20101), excessive synthesis of poly ADP\u2010ribose polymer, mitochondrial depolarization, and nuclear translocation of apoptosis\u2010inducing factor, observed in various neurodegenerative disorders but rarely reported in epilepsy. We aimed to investigate whether parthanatos participates in the mechanism of seizure\u2010induced hippocampal neuronal death.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Glutamate\u2010mediated excitotoxicity cell model was used to study the mechanism of seizure\u2010induced cell injury. Injection of kainic acid into the amygdala was used to establish the epileptic rat model. Corresponding biochemical tests were carried out on hippocampal tissues and HT22 cells following indicated treatments.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In vitro, glutamate time\u2010dependently induced HT22 cell death, accompanied by parthanatos\u2010related biochemical events. Pretreatment with PJ34 (PARP\u20101 inhibitor) or small interfering RNA\u2010mediated PARP\u20101 knockdown effectively protected HT22 cells against glutamate\u2010induced toxic effects and attenuated parthanatos\u2010related biochemical events. Application of the antioxidant N\u2010acetylcysteine (NAC) rescued HT22 cell death and reversed parthanatos\u2010related biochemical events. In vivo, PJ34 and NAC afforded protection against SE\u2010induced hippocampal neuronal damage and inhibited parthanatos\u2010related biochemical events.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Parthanatos participates in glutamate\u2010induced HT22 cell injury and hippocampal neuronal damage in rats following epileptic seizures. ROS might be the initiating factor during parthanatos.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.13934","type":"journal-article","created":{"date-parts":[[2022,8,1]],"date-time":"2022-08-01T06:44:50Z","timestamp":1659336290000},"page":"2032-2043","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Parthanatos participates in glutamate\u2010mediated <scp>HT22<\/scp> cell injury and hippocampal neuronal death in kainic acid\u2010induced status epilepticus rats"],"prefix":"10.1111","volume":"28","author":[{"given":"Xue","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Neurology and Neuroscience Center First Hospital of Jilin University  Changchun Jilin People's Republic of China"},{"name":"Department of Neurology Beijing Friendship Hospital, Capital Medical University  Beijing People's Republic of 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