Genistein inhibited ammonia induced astrocyte swelling by inhibiting NF-[kappa]B activation-mediated nitric oxide formation
Our previous study has indicated the involvement of epidermal growth factor receptor (EGFR) transactivation in ammonia-induced astrocyte swelling, which represents a major pathogenesis of brain edema in hepatic encephalopathy. In this study, we examined the effect of genistein, a naturally occurred...
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Veröffentlicht in: | Metabolic brain disease 2017-06, Vol.32 (3), p.841 |
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description | Our previous study has indicated the involvement of epidermal growth factor receptor (EGFR) transactivation in ammonia-induced astrocyte swelling, which represents a major pathogenesis of brain edema in hepatic encephalopathy. In this study, we examined the effect of genistein, a naturally occurred broad-spectrum protein tyrosine kinase (PTK) inhibitor, on ammonia-induced cell swelling. We found that genistein pretreatment significantly prevented ammonia-induced astrocyte swelling. Mechanistically, ammonia triggered EGFR/extracellular signal-regulated kinase (ERK) association and subsequent ERK phosphorylation were alleviated by genistein pretreatment. Moreover, ammonia-induced NF-[kappa]B nuclear location, iNOS expression, and consequent NO production were all prevented by AG1478 and genistein pretreatment. This study suggested that genistein could alleviate ammonia-induced astrocyte swelling, which may be, at least partly, related to its PTK-inhibiting activity and repression of NF-[kappa]B mediated iNOS-derived NO accumulation. |
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This study suggested that genistein could alleviate ammonia-induced astrocyte swelling, which may be, at least partly, related to its PTK-inhibiting activity and repression of NF-[kappa]B mediated iNOS-derived NO accumulation.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-017-9975-6</identifier><language>eng</language><publisher>New York: Springer Nature B.V</publisher><subject>Activation analysis ; Ammonia ; Brain ; Cell size ; Edema ; Enzyme inhibitors ; Epidermal growth factor ; Epidermal growth factor receptors ; Extracellular signal-regulated kinase ; Genistein ; Hepatic encephalopathy ; NF-κB protein ; Nitric oxide ; Nitric-oxide synthase ; Pathogenesis ; Phosphorylation ; Protein-tyrosine kinase ; Swelling ; Tyrosine</subject><ispartof>Metabolic brain disease, 2017-06, Vol.32 (3), p.841</ispartof><rights>Metabolic Brain Disease is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids></links><search><creatorcontrib>Dai, Hongliang</creatorcontrib><creatorcontrib>Jia, Guizhi</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Liang, Chunguang</creatorcontrib><creatorcontrib>Han, Siyu</creatorcontrib><creatorcontrib>Chu, Minghui</creatorcontrib><creatorcontrib>Mei, Xifan</creatorcontrib><title>Genistein inhibited ammonia induced astrocyte swelling by inhibiting NF-[kappa]B activation-mediated nitric oxide formation</title><title>Metabolic brain disease</title><description>Our previous study has indicated the involvement of epidermal growth factor receptor (EGFR) transactivation in ammonia-induced astrocyte swelling, which represents a major pathogenesis of brain edema in hepatic encephalopathy. 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subjects | Activation analysis Ammonia Brain Cell size Edema Enzyme inhibitors Epidermal growth factor Epidermal growth factor receptors Extracellular signal-regulated kinase Genistein Hepatic encephalopathy NF-κB protein Nitric oxide Nitric-oxide synthase Pathogenesis Phosphorylation Protein-tyrosine kinase Swelling Tyrosine |
title | Genistein inhibited ammonia induced astrocyte swelling by inhibiting NF-[kappa]B activation-mediated nitric oxide formation |
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