NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis
Nuclear receptor subfamily 4 group A1 (NR4A1) is an orphan nuclear receptor, which is expressed in the majority of cells. NR4A1 expression in peripheral blood mononuclear cells is low during the preclinical stage of multiple sclerosis. Knockout of the Nr4a1 gene in mice can aggravate the symptoms of...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2022-01-01
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| Series: | Neural Regeneration Research |
| Subjects: | |
| Online Access: | http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=12;spage=2765;epage=2770;aulast=Yu |
| _version_ | 1811217514446716928 |
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| author | Hai-Zhen Yu Bing-Qing Zhu Lin Zhu Shuo Li Li-Mei Wang |
| author_facet | Hai-Zhen Yu Bing-Qing Zhu Lin Zhu Shuo Li Li-Mei Wang |
| author_sort | Hai-Zhen Yu |
| collection | DOAJ |
| description | Nuclear receptor subfamily 4 group A1 (NR4A1) is an orphan nuclear receptor, which is expressed in the majority of cells. NR4A1 expression in peripheral blood mononuclear cells is low during the preclinical stage of multiple sclerosis. Knockout of the Nr4a1 gene in mice can aggravate the symptoms of experimental autoimmune encephalomyelitis (EAE), which is an animal model of multiple sclerosis. In this study, we intragastrically administered the NR4A1 agonist cytosporone B (Csn-B) to mice after inducing EAE. After treatment with Csn-B, the clinical symptoms in the EAE mice were substantially attenuated compared with that in PBS-treated control mice. The percentages of CD4+ T cells and F4/80+ cells in the central nervous system were decreased. In addition, interferon-γ and interleukin-17 production by proinflammatory Th1/Th17 cells in the central nervous system and interferon-γ levels in splenocytes were decreased after Csn-B treatment. These findings suggest that the NR4A1 agonist Csn-B can alleviate nerve injury after EAE induction, and, therefore, may be useful as a potential treatment for multiple sclerosis. |
| first_indexed | 2024-04-12T06:56:07Z |
| format | Article |
| id | doaj.art-877dd1548eed4a34ab6ec272026a91f8 |
| institution | Directory Open Access Journal |
| issn | 1673-5374 |
| language | English |
| last_indexed | 2024-04-12T06:56:07Z |
| publishDate | 2022-01-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Neural Regeneration Research |
| spelling | doaj.art-877dd1548eed4a34ab6ec272026a91f82022-12-22T03:43:08ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742022-01-0117122765277010.4103/1673-5374.339492NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosisHai-Zhen YuBing-Qing ZhuLin ZhuShuo LiLi-Mei WangNuclear receptor subfamily 4 group A1 (NR4A1) is an orphan nuclear receptor, which is expressed in the majority of cells. NR4A1 expression in peripheral blood mononuclear cells is low during the preclinical stage of multiple sclerosis. Knockout of the Nr4a1 gene in mice can aggravate the symptoms of experimental autoimmune encephalomyelitis (EAE), which is an animal model of multiple sclerosis. In this study, we intragastrically administered the NR4A1 agonist cytosporone B (Csn-B) to mice after inducing EAE. After treatment with Csn-B, the clinical symptoms in the EAE mice were substantially attenuated compared with that in PBS-treated control mice. The percentages of CD4+ T cells and F4/80+ cells in the central nervous system were decreased. In addition, interferon-γ and interleukin-17 production by proinflammatory Th1/Th17 cells in the central nervous system and interferon-γ levels in splenocytes were decreased after Csn-B treatment. These findings suggest that the NR4A1 agonist Csn-B can alleviate nerve injury after EAE induction, and, therefore, may be useful as a potential treatment for multiple sclerosis.http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=12;spage=2765;epage=2770;aulast=Yucytosporone b (csn-b); experimental autoimmune encephalomyelitis; macrophages; microglia; multiple sclerosis; nr4a1 agonist; nr4a1; th1; th17; treatment |
| spellingShingle | Hai-Zhen Yu Bing-Qing Zhu Lin Zhu Shuo Li Li-Mei Wang NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis Neural Regeneration Research cytosporone b (csn-b); experimental autoimmune encephalomyelitis; macrophages; microglia; multiple sclerosis; nr4a1 agonist; nr4a1; th1; th17; treatment |
| title | NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis |
| title_full | NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis |
| title_fullStr | NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis |
| title_full_unstemmed | NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis |
| title_short | NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis |
| title_sort | nr4a1 agonist cytosporone b attenuates neuroinflammation in a mouse model of multiple sclerosis |
| topic | cytosporone b (csn-b); experimental autoimmune encephalomyelitis; macrophages; microglia; multiple sclerosis; nr4a1 agonist; nr4a1; th1; th17; treatment |
| url | http://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=12;spage=2765;epage=2770;aulast=Yu |
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