دورية أكاديمية
N-acetyldopamine dimer inhibits neuroinflammation through the TLR4/NF-κB and NLRP3/Caspase-1 pathways
| العنوان: | N-acetyldopamine dimer inhibits neuroinflammation through the TLR4/NF-κB and NLRP3/Caspase-1 pathways |
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| المؤلفون: | Huang Lijun, Gong Leiqiang, Huo Xueyan, Lei Lirong, Zhang Qi, Hu Yunjie, Kuang Qixuan, Gui Yu, Dai Yifei, Gu Yucheng, Deng Yun, Wang Dong, Guo Dale |
| المصدر: | Acta Biochimica et Biophysica Sinica, Vol 55, Pp 23-33 (2022) |
| بيانات النشر: | China Science Publishing & Media Ltd., 2022. |
| سنة النشر: | 2022 |
| المجموعة: | LCC:Biochemistry LCC:Genetics |
| مصطلحات موضوعية: | N-acetyldopamine dimer, neuroinflammation, TLR4/NF-κB pathway, NLRP3/Caspase-1 pathway, surface plasmon resonance assay, Biochemistry, QD415-436, Genetics, QH426-470 |
| الوصف: | Neuroinflammation mediated by microglia is an important pathophysiological mechanism in neurodegenerative diseases. However, there is a lack of effective drugs to treat neuroinflammation. N-acetyldopamine dimer (NADD) is a natural compound from the traditional Chinese medicine Isaria cicada. In our previous study, we found that NADD can attenuate DSS-induced ulcerative colitis by suppressing the NF-κB and MAPK pathways. Does NADD inhibit neuroinflammation, and what is the target of NADD? To answer this question, lipopolysaccharide (LPS)-stimulated BV-2 microglia was used as a cell model to investigate the effect of NADD on neuroinflammation. Nitric oxide (NO) detection, reactive oxygen species (ROS) detection and enzyme-linked immunosorbent assay (ELISA) results show that NADD attenuates inflammatory signals and proinflammatory cytokines in LPS-stimulated BV-2 microglia, including NO, ROS, tumor necrosis factor (TNF)-α, interleukin (IL)-1β and interleukin-6 (IL-6). Western blot analysis show that NADD inhibits the protein levels of Toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), NOD-like receptor thermal protein domain associated protein 3 (NLRP3), ASC and cysteinyl aspartate specific proteinase (Caspase)-1, indicating that NADD may inhibit neuroinflammation through the TLR4/NF-κB and NLRP3/Caspase-1 signaling pathways. In addition, surface plasmon resonance assays and molecular docking demonstrate that NADD binds with TLR4 directly. Our study reveals a new role of NADD in inhibiting the TLR4/NF-κB and NLRP3/Caspase-1 pathways, and shows that TLR4-MD2 is the direct target of NADD, which may provide a potential therapeutic candidate for the treatment of neuroinflammation. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1672-9145 |
| العلاقة: | https://doaj.org/toc/1672-9145Test |
| DOI: | 10.3724/abbs.2022116 |
| الوصول الحر: | https://doaj.org/article/6cc746c4b9164389b7f33785f962963aTest |
| رقم الانضمام: | edsdoj.6cc746c4b9164389b7f33785f962963a |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 16729145 |
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| DOI: | 10.3724/abbs.2022116 |