The novel small molecule TPN10518 alleviates EAE pathogenesis by inhibiting AP1 to depress Th1/Th17 cell differentiation
文献类型：期刊论文
| 作者 | Xie, Ling1; Lv, Jie1; Saimaier, Kaidireya1; Han, Sanxing1; Han, Mengyao1; Wang, Chun1; Liu, Guangyu1; Zhuang, Wei1; Jiang, Xiangrui2,3 ; Du, Changsheng1,4
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| 刊名 | INTERNATIONAL IMMUNOPHARMACOLOGY
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| 出版日期 | 2023-10-01 |
| 卷号 | 123页码:12 |
| 关键词 | TPN10518 Th1/Th17 cells AP1 Experimental autoimmune encephalomyelitis |
| ISSN号 | 1567-5769 |
| DOI | 10.1016/j.intimp.2023.110787 |
| 通讯作者 | Du, Changsheng(ducs2015@163.com) |
| 英文摘要 | Multiple sclerosis (MS) is one of the most common autoimmune diseases of central nervous system (CNS) demyelination. Experimental autoimmune encephalomyelitis (EAE) is the most classic animal model for simulating the onset of clinical symptoms in MS. Previous research has reported the anti-inflammatory effects of artemisinin on autoimmune diseases. In our study, we identified a novel small molecule, TPN10518, an artemisinin derivative, which plays a protective role on the EAE model. We found that TPN10518 reduced CNS inflammatory cell infiltration and alleviated clinical symptoms of EAE. In addition, TPN10518 downregulated the production of Th1 and Th17 cells in vivo and in vitro, and decrease the levels of related chemokines. RNA-seq assay combined with the experimental results demonstrated that TPN10518 lowered the mRNA and protein levels of the AP1 subunits c-Fos and c-Jun in EAE mice. It was further confirmed that TPN10518 was dependent on AP1 to inhibit the differentiation of Th1 and Th17 cells. The results suggest that TPN10518 reduces the production of Th1 and Th17 cells through inhibition of AP1 to alleviate the severity of EAE disease. It is expected to be a potential drug for the treatment of MS. |
| WOS关键词 | MULTIPLE-SCLEROSIS ; INTERFERON-GAMMA ; T-CELLS ; BRAIN ATROPHY ; INFLAMMATION ; ARTEMISININ ; ARTESUNATE ; INTERLEUKIN-12 ; CHEMOKINE ; SYMPTOMS |
| 资助项目 | National Natural Science Foundation of China[32070768] ; National Natural Science Foundation of China[32270754] |
| WOS研究方向 | Immunology ; Pharmacology & Pharmacy |
| 语种 | 英语 |
| WOS记录号 | WOS:001062695300001 |
| 出版者 | ELSEVIER |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/306131]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Du, Changsheng |
| 作者单位 | 1.Tongji Univ, Putuo Peoples Hosp, Sch Life Sci & Technol, Shanghai Key Lab Signaling & Dis Res, Shanghai, Peoples R China 2.Univ Chinese Acad Sci, Beijing, Peoples R China 3.Chinese Acad Sci, CAS Key Lab Receptor Res, Shanghai Inst Mat Med, Shanghai, Peoples R China 4.Tongji Univ, Putuo Peoples Hosp, Sch Life Sci & Technol, Shanghai Key Lab Signaling & Dis Res, Shanghai 200092, Peoples R China |
| 推荐引用方式 GB/T 7714 | Xie, Ling,Lv, Jie,Saimaier, Kaidireya,et al. The novel small molecule TPN10518 alleviates EAE pathogenesis by inhibiting AP1 to depress Th1/Th17 cell differentiation[J]. INTERNATIONAL IMMUNOPHARMACOLOGY,2023,123:12. |
| APA | Xie, Ling.,Lv, Jie.,Saimaier, Kaidireya.,Han, Sanxing.,Han, Mengyao.,...&Du, Changsheng.(2023).The novel small molecule TPN10518 alleviates EAE pathogenesis by inhibiting AP1 to depress Th1/Th17 cell differentiation.INTERNATIONAL IMMUNOPHARMACOLOGY,123,12. |
| MLA | Xie, Ling,et al."The novel small molecule TPN10518 alleviates EAE pathogenesis by inhibiting AP1 to depress Th1/Th17 cell differentiation".INTERNATIONAL IMMUNOPHARMACOLOGY 123(2023):12. |
入库方式： OAI收割
来源：上海药物研究所
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