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Sinapic Acid Attenuates the Neuroinflammatory Response by Targeting AKT and MAPK in LPS-Activated Microglial Models

  • Tianqi Huang (Division of Bio-Medical Science & Technology, Korea Institute of Science and Technology (KIST) School, Korea University of Science and Technology (UST)) ;
  • Dong Zhao (Division of Bio-Medical Science & Technology, Korea Institute of Science and Technology (KIST) School, Korea University of Science and Technology (UST)) ;
  • Sangbin Lee (Department of Integrative Biological Sciences and Industry, Sejong University) ;
  • Gyochang Keum (Division of Bio-Medical Science & Technology, Korea Institute of Science and Technology (KIST) School, Korea University of Science and Technology (UST)) ;
  • Hyun Ok Yang (Department of Integrative Biological Sciences and Industry, Sejong University)
  • Received : 2022.07.05
  • Accepted : 2022.10.28
  • Published : 2023.05.01

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 inflammation-related 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

Acknowledgement

This work was funded and supported by the Bio-Synergy Research Project (NRF-2012M3A9C4048793) of the Ministry of Science, ICT and Future Planning through the National Research Foundation of the Republic of Korea. This work was also supported by the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) funded by the Ministry of Health & Welfare, Republic of Korea (Grant Number: HI18C1860), and by the Korea Institute of Science and Technology (KIST) Institutional Programs (Grant No. 2E31512).

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