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Here, we aimed to determine the protective action of BHS on hippocampal neurons against oxidative stress. We investigated the functional effect of BHS on a scopolamine\u2010induced mouse model, and molecular analysis was performed in glutamate\u2010induced HT22 cells. We observed that BHS administration ameliorated memory dysfunction in scopolamine\u2010treated mice. BHS administration also increased neuronal survival and acetylcholine activity and phosphorylation of extracellular signal\u2010regulated kinase (ERK) and cAMP response element\u2010binding protein (CREB) in the hippocampus of mice. In hippocampal cells, BHS treatment rescued glutamate\u2010induced cytotoxicity, apoptosis, and oxidative stress. We observed an increase of HO\u20101 and a decrease of Nrf2 protein expression in glutamate\u2010induced oxidative stress; however, the expression level of these proteins was significantly rescued by BHS treatment. BHS treatment also regulated phosphorylation of p38, p53, ERK, and CREB. Therefore, our data indicated that BHS may reduce oxidative stress through regulation of ERK\u2010CREB and p38\u2010p53 signaling in the hippocampus, resulting in decreased neuronal damage and improved memory in rodent models of neurodegenerative disease.<\/jats:p>","DOI":"10.1155\/2021\/6970578","type":"journal-article","created":{"date-parts":[[2021,12,3]],"date-time":"2021-12-03T02:50:09Z","timestamp":1638499809000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Banhasasim\u2010Tang Ameliorates Spatial Memory by Suppressing Oxidative Stress through Regulation of ERK\/p38 Signaling in Hippocampus of Mice"],"prefix":"10.1155","volume":"2021","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6008-271X","authenticated-orcid":false,"given":"Malk 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