Objective: In this study, we aimed to investigate hyperin’s potentiality in inhibition of neuroinflammation.

Background: Hyperin is an active compound isolated from Rhododendron brachycarpum G. Don (Ericaceae).

Methods: BV2 microglial cells were pretreated with hyperin and stimulated with lipopolysaccharide (LPS).

Results: The results showed that hyperin significantly inhibited LPS-induced production of nitric oxide (NO) and pro-inflammatory cytokines such as TNF-α and IL-1β. Further analysis showed that inducible nitric oxide synthase (iNOS) and mRNA expression of TNF-α and IL-1β were attenuated by hyperin pretreatment. Analyses in signaling pathways demonstrated that hyperin led to suppression of LPS-induced p38 MAPK and p65/NFκB activation, but had little effect on the activation of JNK1/2 and Erk1/2. Interference with specific inhibitors revealed that hyperin attenuated the LPS-induced production of NO, TNF-α and IL-1β via both p38 and NFκB pathways. The inhibitory role of hyperin on cytokine production was further confirmed using primary microglia cells. By conditioned media culture hyperin suppressed the microglia-mediated neurotoxicity.

Conclusions: Collectively, our data suggest that hyperin may serve as an anti-inflammatory agent and contribute to the suppression of neuroinflammation in disorders such as Parkinson’s disease.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/hyperin-inhibits-lipopolysaccharide-induced-microglia-activation-through-p38-and-nfb-signaling/