Anti-Inflammatory Activity of Panduratin A against LPS-Induced Microglial Activation

Abstract

Uncontrolled and excessive microglial activation is known to contribute to inflammation-mediated neurodegeneration. Therefore, reducing neurotoxic microglial activation may serve as a new approach to preventing neurodegeneration. Here, we investigated the anti-inflammatory effects of panduratin A against microglial activation induced by lipopolysaccharides (LPS) in the SIMA9 microglial cell line. We initially examined the anti-inflammatory properties of panduratin A by measuring LPS-induced nitric oxide (NO) production and the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). Panduratin A significantly reduced NO levels and pro-inflammatory cytokines’ production and secretion. In addition, panduratin A enhanced the production of anti-inflammatory cytokines IL-4 and IL-10. The anti-inflammatory effects of panduratin A are related to the suppression of the NF-κB signaling pathway. Together, these results demonstrate the anti-inflammatory properties of panduratin A against LPS-induced microglial activation, suggesting panduratin A has the potential to be further developed as a new agent for the prevention of neuroinflammation-associated neurodegenerative diseases.

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“…The NF-κB signaling pathway is one of the general signal transduction pathways that mediate gene expression of proinflammatory and antiapoptotic factors, cell proliferation, differentiation, adhesion, migration and angiogenesis [ 14 ]. The hyperactivation of NF-κB signaling is a hallmark of many types of cancer [ 14 ] and inflammatory-associated pathologies [ 14 , 15 ]. Additionally, the chronic inflammation associated with upregulation of NF-κB signaling is a common feature of multiple neurodegenerative diseases [ 16 ].…”

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“…Simultaneously, panduratin A increased the release of the anti-inflammatory cytokines IL-4 and IL-10, effectively attenuating the pro-inflammatory stage in neuroinflammatory diseases [19] , [20] . An in vitro study focused on the prevention of neuroinflammation-associated neurodegenerative diseases found that panduratin A counteracted lipopolysaccharide (LPS)-induced microglial activation in the spontaneous immortalized microglia-A9 (SIM-A9) cell line by reducing NO levels and pro-inflammatory cytokine production, and secretion [21] . Pinostrobin ( Fig.…”