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Effective suppression of nitric oxide production by HX106N through transcriptional control of heme oxygenase-1
DC Field | Value | Language |
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dc.contributor.author | Lee, Doo Suk | - |
dc.contributor.author | Kim, Binna N. | - |
dc.contributor.author | Lim, Seonung | - |
dc.contributor.author | Lee, Junsub | - |
dc.contributor.author | Kim, Jiyoung | - |
dc.contributor.author | Jeong, Jae-Gyun | - |
dc.contributor.author | Kim, Sunyoung | - |
dc.date.accessioned | 2024-05-14T01:27:36Z | - |
dc.date.available | 2024-05-14T01:27:36Z | - |
dc.date.created | 2018-10-31 | - |
dc.date.created | 2018-10-31 | - |
dc.date.issued | 2015-09 | - |
dc.identifier.citation | Experimental Biology and Medicine, Vol.240 No.9, pp.1136-1146 | - |
dc.identifier.issn | 1535-3702 | - |
dc.identifier.uri | https://hdl.handle.net/10371/201669 | - |
dc.description.abstract | Heme oxygenase-1 (HO-1) has been suggested to be a key neuroprotective enzyme because of its widespread distribution in the brain as well as its strong antioxidative effects. HX106N, a water-soluble botanical formulation, has previously been demonstrated to prevent amyloid b-induced memory impairment and oxidative stress in mice by upregulating HO-1 levels. In this study, the underlying molecular mechanisms of HX106N-induced HO-1 expression were investigated using BV-2 cells, a murine microglial cell line, and primary microglia. Treatment with HX106N induced the expression of HO-1 at the transcriptional level through the stress-responsive element-containing enhancer present in the ho-1 promoter. Nuclear factor E2-related factor 2 (Nrf2) was activated in cells treated with HX106N. The results from knockdown assay showed that small interfering RNA of Nrf2 attenuated HX106N-mediated HO-1 expression. Pharmacological inhibitors of p38 and JNK mitogen-activated protein kinases suppressed the HX106N-mediated induction of HO-1. The NF-kappa B signaling pathway was activated by HX106N and played a role in HX106N-induced HO-1 expression. Furthermore, HO-1 and one of its by-products during the enzymatic degradation of heme, CO, were found to be involved in HX106N-mediated suppression of NO production. Taken together, these data indicate that HX106N exerts potent antioxidative effects by increasing the expression of HO-1 through multiple signaling pathways, leading to the suppression of NO production. | - |
dc.language | 영어 | - |
dc.publisher | Society for Experimental Biology and Medicine | - |
dc.title | Effective suppression of nitric oxide production by HX106N through transcriptional control of heme oxygenase-1 | - |
dc.type | Article | - |
dc.identifier.doi | 10.1177/1535370214567612 | - |
dc.citation.journaltitle | Experimental Biology and Medicine | - |
dc.identifier.wosid | 000361054600002 | - |
dc.identifier.scopusid | 2-s2.0-84960355128 | - |
dc.citation.endpage | 1146 | - |
dc.citation.number | 9 | - |
dc.citation.startpage | 1136 | - |
dc.citation.volume | 240 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Kim, Sunyoung | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | ACTIVATED PROTEIN-KINASE | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | THERAPEUTIC TARGET | - |
dc.subject.keywordPlus | INOS EXPRESSION | - |
dc.subject.keywordPlus | CARBON-MONOXIDE | - |
dc.subject.keywordPlus | NO PRODUCTION | - |
dc.subject.keywordPlus | BASAL LEVEL | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | ANTIOXIDANT | - |
dc.subject.keywordAuthor | HX106N | - |
dc.subject.keywordAuthor | heme oxygenase-1 | - |
dc.subject.keywordAuthor | nuclear factor E2-related factor 2 | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordAuthor | nitric oxide | - |
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