دورية أكاديمية
Anti-inflammatory and antioxidant mechanisms of coniferaldehyde in lipopolysaccharide-induced neuroinflammation: Involvement of AMPK/Nrf2 and TAK1/MAPK/NF-κB signaling pathways.
| العنوان: | Anti-inflammatory and antioxidant mechanisms of coniferaldehyde in lipopolysaccharide-induced neuroinflammation: Involvement of AMPK/Nrf2 and TAK1/MAPK/NF-κB signaling pathways. |
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| المؤلفون: | Park JM; Department of Molecular Medicine, Inflammation-Cancer Microenvironment Research Center, School of Medicine, Ewha Womans University, Seoul, South Korea., Park JE; Department of Molecular Medicine, Inflammation-Cancer Microenvironment Research Center, School of Medicine, Ewha Womans University, Seoul, South Korea., Park JS; Department of Molecular Medicine, Inflammation-Cancer Microenvironment Research Center, School of Medicine, Ewha Womans University, Seoul, South Korea., Leem YH; Department of Molecular Medicine, Inflammation-Cancer Microenvironment Research Center, School of Medicine, Ewha Womans University, Seoul, South Korea., Kim DY; Department of Molecular Medicine, Inflammation-Cancer Microenvironment Research Center, School of Medicine, Ewha Womans University, Seoul, South Korea., Hyun JW; Department of Biochemistry, College of Medicine, and Jeju Research Center for Natural Medicine, Jeju National University, Jeju, South Korea., Kim HS; Department of Molecular Medicine, Inflammation-Cancer Microenvironment Research Center, School of Medicine, Ewha Womans University, Seoul, South Korea. Electronic address: hskimp@ewha.ac.kr. |
| المصدر: | European journal of pharmacology [Eur J Pharmacol] 2024 Sep 15; Vol. 979, pp. 176850. Date of Electronic Publication: 2024 Jul 25. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Science Country of Publication: Netherlands NLM ID: 1254354 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-0712 (Electronic) Linking ISSN: 00142999 NLM ISO Abbreviation: Eur J Pharmacol Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2005- : Amsterdam : Elsevier Science Original Publication: Amsterdam, North Holland Pub. Co. |
| مواضيع طبية MeSH: | Lipopolysaccharides* , NF-E2-Related Factor 2*/metabolism , Antioxidants*/pharmacology , Anti-Inflammatory Agents*/pharmacology , Anti-Inflammatory Agents*/therapeutic use , NF-kappa B*/metabolism , AMP-Activated Protein Kinases*/metabolism , MAP Kinase Kinase Kinases*/metabolism , Microglia*/drug effects , Microglia*/metabolism , Signal Transduction*/drug effects, Animals ; Mice ; Male ; Cell Line ; Oxidative Stress/drug effects ; Neuroinflammatory Diseases/drug therapy ; Neuroinflammatory Diseases/metabolism ; Neuroinflammatory Diseases/chemically induced ; Acrolein/analogs & derivatives ; Acrolein/pharmacology ; Cytokines/metabolism ; Reactive Oxygen Species/metabolism |
| مستخلص: | Microglia are primarily involved in inflammatory reactions and oxidative stress in the brain; as such reducing microglial activation has been proposed as a potential therapeutic strategy for neurodegenerative disorders. Herein, we investigated the anti-inflammatory and antioxidant activities of coniferaldehyde (CFA), a naturally occurring cinnamaldehyde derivative, on activated microglia to evaluate its therapeutic potential. CFA inhibited the production of nitric oxide (NO) and proinflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1β, and IL-6, in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. CFA also inhibited intracellular reactive oxygen species levels and oxidative stress markers such as 4-HNE and 8-OHdG. Detailed mechanistic studies showed that CFA exerted anti-inflammatory effects by inhibiting TAK1-mediated MAP kinase/NF-κB activation and upregulating AMPK signaling pathways. In addition, CFA exerted antioxidant effects by inhibiting the NADPH oxidase subunits and by increasing the expression of antioxidant enzymes such as HO-1, NQO1, and catalase by upregulating Nrf2 signaling. Finally, we confirmed the effects of CFA on the brains of the LPS-injected mice. CFA inhibited microglial activation and the expression of proinflammatory markers and increased Nrf2-driven antioxidant enzymes. Furthermore, CFA inhibited the production of 4-HNE and 8-OHdG in the brains of LPS-injected mice. As a result, CFA's significant anti-inflammatory and antioxidant properties may have therapeutic applications in neuroinflammatory disorders related with oxidative stress and microglial activation. Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare. (Copyright © 2024 Elsevier B.V. All rights reserved.) |
| فهرسة مساهمة: | Keywords: Antioxidant enzymes; Coniferaldehyde; Microglia; Molecular mechanism; Neuroinflammation |
| المشرفين على المادة: | 0 (Lipopolysaccharides) 0 (NF-E2-Related Factor 2) 0 (Antioxidants) 0 (Anti-Inflammatory Agents) EC 2.7.11.25 (MAP kinase kinase kinase 7) 0 (NF-kappa B) EC 2.7.11.31 (AMP-Activated Protein Kinases) EC 2.7.11.25 (MAP Kinase Kinase Kinases) 0 (Nfe2l2 protein, mouse) 7864XYD3JJ (Acrolein) 0 (Cytokines) 0 (Reactive Oxygen Species) |
| تواريخ الأحداث: | Date Created: 20240726 Date Completed: 20240816 Latest Revision: 20240822 |
| رمز التحديث: | 20240823 |
| DOI: | 10.1016/j.ejphar.2024.176850 |
| PMID: | 39059571 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1879-0712 |
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| DOI: | 10.1016/j.ejphar.2024.176850 |