Biomolecules & Therapeutics  https://doi.org/10.4062/biomolther.2022.092
Sinapic Acid Attenuates the Neuroinflammatory Response by Targeting AKT and MAPK in LPS-Activated Microglial Models
Tianqi Huang1,2,3, Dong Zhao1, Sangbin Lee3, Gyochang Keum1,2,* and Hyun Ok Yang3,*
1Division of Bio-Medical Science & Technology, Korea Institute of Science and Technology (KIST) School, Korea University of Science and Technology (UST), Seoul 02792,
2Brain Research Institute, Korea Institute of Science and Technology (KIST), Seoul 02792,
3Department of Integrative Biological Sciences and Industry, Sejong University, Seoul 05006, Republic of Korea
*E-mail: hoyang@sejong.ac.kr (Yang HO), gkeum@kist.re.kr (Keum G)
Tel: +82-2-3408-1959 (Yang HO), +82-2-958-5148 (Keum G)
Fax: +82-2-3048-4336 (Yang HO), +82-2-958-5189 (Keum G)
Received: July 5, 2022; Revised: October 19, 2022; Accepted: October 28, 2022; Published online: November 25, 2022.
© The Korean Society of Applied Pharmacology. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Sinapic acid (SA) is a phenolic acid that is widely distributed in fruits and vegetables, which has various bioactivities, such as antidiabetic, anticancer and anti-inflammatory functions. Over-activated microglial is involved in the development progress of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. The objective of this study was to investigate the effect of SA in microglia neuroinflammation models. Our results demonstrated that SA inhibited secretion of the nitric oxide (NO) and interleukin (IL)-6, reduced the expression of inducible nitric oxide synthase (iNOS) and enhanced the release of IL-10 in a dose-dependent manner. Besides, our further investigation revealed that SA attenuated the phosphorylation of AKT and MAPK cascades in LPS-induced microglia. Consistently, oral administration of SA in mouse regulated the production of inflammationrelated cytokines and also suppressed the phosphorylation of MAPK cascades and AKT in the mouse cerebral cortex. These results suggested that SA may be a possible therapy candidate for anti-inflammatory activity by targeting the AKT/MAPK signaling pathway.
Keywords: Sinapic acid, Neuroinflammation, BV-2 microglia, Anti-inflammation, MAPK/AKT signaling pathway

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