Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 111, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2022.109118
Keywords
Chrysin; Neuroinflammation; Fyn; NF -KB; NLRP3
Categories
Funding
- National Natural Science Foundation of China [82074047, 81903697]
- Yantai Double-hundred Talent Plan
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The study demonstrates that chrysin inhibits the activation of Fyn kinase, alleviating neuroinflammation-induced neuron damage and behavior deficits. It also reduces the expression of inflammatory molecules by inhibiting microglial activation.
Fyn, a non-receptor tyrosine kinase, plays an important role in microglial-mediated neuroinflammation and may serve as a candidate therapeutic target for neuropsychiatric diseases. In this study, we discovered that chrysin, a natural flavonoid compound, suppressed the activation of Fyn kinase and further alleviated neuroinflammation-induced neuron damage and behavior deficits. Functionally, chrysin improved lipopolysaccharide (LPS)-induced memory impairment and depressive behaviors in mice, it also protected against LPS-induced neuronal degen-eration and loss and synaptic defects in mice. Our study demonstrated that chrysin inhibited the activation of microglia and reduced the expression of NLRP3 and IL-1 beta. Furthermore, our data indicated that chrysin blocked phosphorylation of Fyn and activation of NF-KB. Transfection with siRNA-Fyn validated that knockdown of Fyn partly abolished the inhibitory effect of chrysin on the expression of the NLRP3 inflammasome and NF-KB activation. Taken together, our findings revealed that chrysin alleviated LPS-induced neuron damage and behavioral deficits by inhibiting the expression of the NLRP3 inflammasome and NF-KB pathway, which might be mediated by inhibition of Fyn.
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