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Genistein (GE) is an isoflavone widely present in leguminous plants, and it was found to exert a wide spectrum of biological activities, including antioxidant, anti\u2010inflammatory, hepatoprotective, neuroprotective, and antimetastatic effects. In this study, the protective effect of GE on chronic sleep deprivation (CSD)\u2010induced cognitive dysfunction was investigated. The mice were subjected to the sleep interruption apparatus and continuously sleep deprived for 25 days. GE was orally administrated (10, 20, and 40 mg\/kg) during the sleep deprivation process totally for 25 days. Cognitive behavioral tests were conducted to study the learning and memory using the object location recognition (OLR) task, novel object recognition (NOR) test, and the Morris water maze (MWM) task. Additionally, the cortex and hippocampus were dissected to measure the oxidative stress markers and the antioxidant element nuclear erythroid\u20102\u2010related factor 2 (Nrf2) and its downstream targets, including glutamate cysteine ligase catalytic, glutamate cysteine ligase modifier, heme oxygenase 1, and quinone oxidoreductase 1, as well as nuclear factor kappa B (NF\u2010\u03baB) p65, nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX\u20102) protein expression. Moreover, the pro\u2010inflammatory cytokines (TNF\u2010\u03b1, interleukin [IL]\u20106, and IL\u20101\u03b2) level was examined in the serum. The current results showed that GE could dose\u2010dependently ameliorate the cognitive deficits of CSD\u2010treated mice in the OLR, NOR, and MWM tasks. In addition, GE treatment significantly elevated the activities of total antioxidant capacity and superoxide dismutase and the level of glutathione and lowered the content of malondialdehyde in the cortex and hippocampus of CSD\u2010treated mice. Furthermore, GE administration effectively activated the antioxidant element Nrf2 and its downstream targets in the cortex and hippocampus of CSD\u2010treated mice. Moreover, GE treatment significantly suppressed CSD\u2010induced NF\u2010\u03baB p65, iNOS, and COX\u20102 activation in the cortex and hippocampus, as well as inhibited CSD\u2010induced pro\u2010inflammatory cytokines (TNF\u2010\u03b1, IL\u20106, and IL\u20101\u03b2) release in the serum. Taken together, all these results suggested that GE has substantial potential as a therapeutic intervention for the alleviation of CSD\u2010induced deleterious effects.<\/jats:p>","DOI":"10.1002\/ptr.6567","type":"journal-article","created":{"date-parts":[[2020,3,2]],"date-time":"2020-03-02T09:36:32Z","timestamp":1583141792000},"page":"846-858","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["Protective effects of Genistein on the cognitive deficits induced by chronic sleep deprivation"],"prefix":"10.1002","volume":"34","author":[{"given":"Cong","family":"Lu","sequence":"first","affiliation":[{"name":"Institute of Food Science and Technology Chinese Academy of Agricultural Sciences (CAAS)  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingwei","family":"Lv","sequence":"additional","affiliation":[{"name":"Research Center for Pharmacology &amp; Toxicology, Institute of Medicinal Plant Development (IMPLAD) Chinese Academy of Medical Sciences (CAMS) and Peking Union Medical College (PUMC)  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ning","family":"Jiang","sequence":"additional","affiliation":[{"name":"Research Center for Pharmacology &amp; 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