NRF2 activation by 2-methoxycinnamaldehyde attenuates inflammatory responses in macrophages via enhancing autophagy fluxopen access
- Authors
- Kim, Bo-Sung; Shin, Minwook; Kim, Kyu-Won; Ha, Ki-Tae; Bae, Sung-Jin
- Issue Date
- Aug-2022
- Publisher
- 생화학분자생물학회
- Keywords
- 2-methoxycinnamaldehyde; Autophagy; Inflammation; Lps; Nrf2
- Citation
- BMB Reports, v.55, no.8, pp 407 - 412
- Pages
- 6
- Journal Title
- BMB Reports
- Volume
- 55
- Number
- 8
- Start Page
- 407
- End Page
- 412
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/151528
- DOI
- 10.5483/BMBRep.2022.55.8.065
- ISSN
- 1976-6696
1976-670X
- Abstract
- A well-controlled inflammatory response is crucial for the recovery from injury and maintenance of tissue homeostasis. The anti-inflammatory response of 2-methoxycinnamaldehyde (2-MCA), a natural compound derived from cinnamon, has been studied; however, the underlying mechanism on macrophage has not been fully elucidated. In this study, LPS-stimulated production of TNF-α and NO was reduced by 2-MCA in macrophages. 2-MCA significantly activated the NRF2 pathway, and expression levels of autophagy-associated proteins in macrophages, including LC3 and P62, were enhanced via NRF2 activation regardless of LPS treatment, suggesting the occurrence of 2-MCA-mediated autophagy. Moreover, evaluation of autophagy flux using luciferase-conjugated LC3 revealed that incremental LC3 and P62 levels are coupled to enhanced autophagy flux. Finally, reduced expression levels of TNF-α and NOS2 by 2-MCA were reversed by autophagy inhibitors, such as bafilomycin A1 and NH4Cl, in LPS-stimulated macrophages. In conclusion, 2-MCA enhances autophagy flux in macrophages via NRF2 activation and consequently reduces LPS-induced inflammation.
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