Abstract
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-κB pathway, as evidenced by decreased phosphorylation of IKK and IκB 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-α 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-κB activation in mice brains. Taken together, DeGA F exhibited remarkable anti-inflammatory effects and promising therapeutic potential for neural inflammation associated diseases.
Highlights
Inflammation is a defense mechanism of the organism to various harmful stimuli, such as irritants, damaged cells, or pathogens [1]
The effect of Deacetyl ganoderic acid F (DeGA F) on BV-2 cell viability was evaluated by using CCK-8 assay
The results indicated that DeGA F was nontoxic to the BV-2 cells up to 48 h (Figure 1B), and morphological changes in the cells were rarely observed in the microscopic analysis
Summary
Inflammation is a defense mechanism of the organism to various harmful stimuli, such as irritants, damaged cells, or pathogens [1]. Inflammation is considered beneficial for self-healing and repairing owing to its function of eliminating the damaged tissues or necrotic cells from the original stimulation and the inflammatory reaction. An excessive or uncontrolled extent of inflammation is detrimental to an organism and may result in inflammatory disorders. Recent mechanistic studies and genetic evidence indicate that immune signal pathway dysregulation in brain; alternation in cytokine secretion, immune cell migration and proliferation, and abnormal phagocytosis and gliosis are common characteristics of neurodegenerative disorders [4]. Microglia, the resident innate immune cells in brain parenchyma, is regarded as the primary cellular mediator of the immune response
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