Yomogin, Isolated from Artemisia iwayomogi, Inhibits Neuroinflammation Stimulated by Lipopolysaccharide via Regulating MAPK Pathwayopen access
- Authors
- Kim, Jin Hee; Ju, In Gyoung; Kim, Namkwon; Huh, Eugene; Son, So-Ri; Hong, Joon Pyo; Choi, Yujin; Jang, Dae Sik; Oh, Myung Sook
- Issue Date
- Jan-2023
- Publisher
- MDPI
- Keywords
- yomogin; neuroinflammation; p38 mitogen-activated protein kinases; JNK mitogen-activated protein kinases; ERK extracellular signal-regulated kinase; Artemisia iwayomogi
- Citation
- ANTIOXIDANTS, v.12, no.1
- Journal Title
- ANTIOXIDANTS
- Volume
- 12
- Number
- 1
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/88239
- DOI
- 10.3390/antiox12010106
- ISSN
- 2076-3921
- Abstract
- Neuroinflammation causes various neurological disorders, including depression and neurodegenerative diseases. Therefore, regulation of neuroinflammation is a promising therapeutic strategy for inflammation-related neurological disorders. This study aimed to investigate whether yomogin, isolated from Artemisia iwayomogi, has anti-neuroinflammatory effects. First, we evaluated the effects of yomogin by assessing pro-inflammatory mediators and cytokines in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. The results showed that yomogin inhibited the increase in neuroinflammatory factors, including nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha, and suppressed phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase and p38, which participate in the mitogen-activated protein kinase (MAPK) pathway. To confirm these effects in vivo, we measured the activation of astrocyte and microglia in LPS-injected mouse brains. Results showed that yomogin treatment decreased astrocyte and microglia activations. Collectively, these results suggest that yomogin suppresses neuroinflammation by regulating the MAPK pathway and it could be a potential candidate for inflammation-mediated neurological diseases.
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