Aucubin suppresses lipopolysaccharide-induced pro-inflammatory responses by blocking the NF-κB translocation signaling pathways in activated microglial cells
- Authors
- Park, Yong Joo; Lim, Ja Young; Kwon, Seung-Hwan; Shin, Myoung Sook
- Issue Date
- Apr-2022
- Publisher
- Elsevier
- Keywords
- Aucubin; Lipopolysaccharide; Microglial cells; Nuclear factor-kappa B; Pro-inflammatory responses
- Citation
- Phytochemistry Letters, v.48, pp.120 - 127
- Journal Title
- Phytochemistry Letters
- Volume
- 48
- Start Page
- 120
- End Page
- 127
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/83805
- DOI
- 10.1016/j.phytol.2022.02.006
- ISSN
- 1874-3900
- Abstract
- Aucubin is an iridoid glycoside with demonstrable hepatoprotective and anti-osteoporotic effects. Herein, using microglial cells and lipopolysaccharide (LPS) to induce inflammatory responses, we studied the signaling pathways involved in the anti-inflammatory action of aucubin and their influence on the expression of several genes known to be involved in inflammation. Aucubin inhibited LPS-stimulated pro-inflammatory responses by suppressing the production of nitric oxide and prostaglandin E2. Furthermore, aucubin inhibited inducible nitric oxide synthase and cyclooxygenase-2 at both the protein and mRNA levels. In addition, aucubin inhibited pro-inflammatory cytokine production in LPS-stimulated BV-2 microglial cells. Subsequent mechanistic studies revealed that aucubin inhibited the LPS-induced activation of nuclear factor-kappa B (NF-κB) translocation and phosphorylation of phosphatidylinositol 3-kinases (PI3K)/Akt as well as of mitogen-activated protein kinases (MAPKs), which are upstream molecules responsible for controlling inflammatory reactions. These results suggest that aucubin may exert anti-neuroinflammatory responses by suppressing the LPS-induced expression of pro-inflammatory mediators by blocking the activation of NF-κB, PI3K/Akt, and MAPK signaling pathways in microglial cells. © 2022 Phytochemical Society of Europe
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