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In this study, we aimed to examine protective properties of AKBA against glutamate\u2010induced neuronal injury. To investigate the effects of AKBA (2.5\u201010\u2009\u00b5M) on glutamate injury in neuron\u2010like cells PC12 and N2a, two treatment regimens (incubation for 2 or 0\u2009hours before glutamate exposure) were used. Then, the 3\u2010(4,5\u2010dimethylthiazol\u20102\u2010yl)\u20102,5\u2010diphenyltetrazolium bromide method was used to determine viability of the cells. Cellular redox status was evaluated using fluorimetry and comet assays. Annexin V\/propidium iodide double staining and Western blot analysis of relative apoptotic proteins were conducted. Based on the results, 24\u2009hours incubation with glutamate (8\u2009mM) increased the cell mortality of PC12 and N2a (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u2009.001). However, AKBA (2.5\u201010\u2009\u00b5M) enhanced the cell viability in both treatment regimens (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u2009.001). Also co\u2010 and pretreatment with AKBA significantly attenuated lipid peroxidation, reactive oxygen species production, and DNA injury (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u2009.05 and\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u2009.001). AKBA also restored the activity of cellular superoxide dismutase under glutamate toxicity; this effect was seen to be more significant during the pretreatment regimen (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009&lt;\u2009.001). Moreover, Western blot analysis indicated that AKBA inhibited glutamate\u2010induced programmed cell death through depressing the elevation of the expression ratio of Bax\/Bcl\u20102 and cleaved\u2010caspase\u20103 proteins, concentration\u2010dependently. Overall, the present findings suggest the neuroprotective activities of AKBA against glutamate\u2010induced cell injury probably by inhibiting oxidative damage and reducing apoptotic cell death.\n                  <\/jats:p>","DOI":"10.1002\/jcb.29413","type":"journal-article","created":{"date-parts":[[2019,10,23]],"date-time":"2019-10-23T05:03:56Z","timestamp":1571807036000},"page":"1778-1789","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["RETRACTED: 3\u2010Acetyl\u201011\u2010keto\u2010\u03b2\u2010boswellic acid attenuated oxidative glutamate toxicity in neuron\u2010like cell lines by apoptosis inhibition"],"prefix":"10.1002","volume":"121","author":[{"given":"Arezoo","family":"Rajabian","sequence":"first","affiliation":[{"name":"Pharmacological Research Center of Medicinal Plants, Faculty of Medicine Mashhad University of Medical Sciences  Mashhad 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