Journal
NUTRIENTS
Volume 12, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/nu12010085
Keywords
deacetyl ganoderic acid F; LPS-induced inflammation; microglia cells; zebrafish; mice
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Funding
- Research Committee of the University of Macau [MYRG2014-00089-ICMS-QRCM, MYRG2018-00239-ICMS]
- Macau Science and Technology Development Fund [162/2017/A3]
- Guangzhou International Science and Technology Cooperation Project [201807010044]
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Microglia mediated neuronal inflammation has been widely reported to be responsible for neurodegenerative disease. Deacetyl ganoderic acid F (DeGA F) is a triterpenoid isolated from Ganoderma lucidum, which is a famous edible and medicinal mushroom used for treatment of dizziness and insomnia in traditional medicine for a long time. In this study the inhibitory effects and mechanisms of DeGA F against lipopolysaccharide (LPS)-induced inflammation both in vitro and in vivo were investigated. On murine microglial cell line BV-2 cells, DeGA F treatment inhibited LPS-triggered NO production and iNOS expression and affected the secretion and mRNA levels of relative inflammatory cytokines. DeGA F inhibited LPS-induced activation of the NF-kappa B pathway, as evidenced by decreased phosphorylation of IKK and I kappa B and the nuclear translocation of P65. In vivo, DeGA F treatment effectively inhibited NO production in zebrafish embryos. Moreover, DeGA F suppressed the serum levels of pro-inflammatory cytokines, including TNF-alpha and IL-6 in LPS-stimulated mice model. DeGA F reduced inflammatory response by suppressing microglia and astrocytes activation and also suppressed LPS-induced NF-kappa B activation in mice brains. Taken together, DeGA F exhibited remarkable anti-inflammatory effects and promising therapeutic potential for neural inflammation associated diseases.
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