Journal
PHYTOMEDICINE
Volume 84, Issue -, Pages -Publisher
ELSEVIER GMBH
DOI: 10.1016/j.phymed.2021.153501
Keywords
Artemisia iwayomogi; Neuroinflammation; Mitogen-activated protein kinases; Nuclear factor kappa B; NLRP3
Categories
Funding
- Medical Research Center Program through the National Research Foundation of Korea - Ministry of Science and ICT [NRF-2017R1A5A2014768]
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This study showed that Artemisiae Iwayomogii Herba (AIH) attenuates neuroinflammation by regulating the NF-kappa B and MAPK pathways, and it may be used for treating neurological diseases. The inhibitory effects of AIH on microglia-mediated neuroinflammation and NLRP3 inflammasome formation were demonstrated both in vitro and in a mouse model.
Background: Neuroinflammation plays a major role in the development of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. The regulation of microglia is an efficient therapeutic approach to controlling neuroinflammation. Purpose: In this study, we aimed to determine whether Artemisiae Iwayomogii Herba (AIH), which is herbal medicine traditionally used for inflammation-related disorders, controls neuroinflammatory responses by regulating the microglia-mediated signaling pathway. Methods: BV-2 microglial cells were treated with AIH and lipopolysaccharides (LPS), then various proinflammatory mediators were analyzed using griess reaction, quantitative reverse-transcription polymerase chain reaction, or western blotting. C57BL/6 J mice were orally administered by AIH for 17 days and intraperitoneally injected with LPS for the last 14 days. The brains were collected and the microglial activation and nucleotide-binding oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing 3 (NLRP3) expression in the cortex and hippocampus were analyzed using immunohistochemistry or western blotting. Results: In BV-2 microglial cells, we found that AIH inhibited nitric oxide (NO) production induced by LPS. AIH also suppressed the expressions of pro-inflammatory mediators, including inducible NO synthase, cyclooxygenase-2, tumor necrosis factor-alpha, and interleukin-6. The study also revealed that the effects of AIH are related to the regulation of the nuclear factor kappa B (NF-kappa B) and the mitogen-activated protein kinase (MAPK) signaling pathway. Additionally, we found that AIH prevented the formation of NLRP3 inflammasomes. Consistent with the results of in vitro studies on the brains of LPS-injected mice, we observed that AIH suppressed microglial activation and NLRP3 expression. Conclusion: Taken together, these results suggest that AIH attenuates neuroinflammation by regulating the NF-kappa B and MAPK pathways, and it may be used for treating neurological diseases.
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