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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

NRF2 activation by 2-methoxycinnamaldehyde attenuates inflammatory responses in macrophages via enhancing autophagy flux
Bo-Sung Kim 1,2,# (Graduate student), Minwook Shin 3,# (Research Professor), Kyu-Won Kim4 (Professor), Ki-Tae Ha 1,2,*,# (Professor), Sung-Jin Bae 5,# (Professor)
1Department of Korean Medical Science, School of Korean Medicine and 2Korean Medical Research Center for Healthy Aging, Pusan National University,
3RNA Therapeutics Institute, University of Massachusetts Chan Medical School,
4College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University,
5Department of Molecular Biology and Immunology, Kosin University College of Medicine
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-メ 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-メ 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.
Abstract, Accepted Manuscript(in press) [Submitted on April 11, 2022, Accepted on June 15, 2022]
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