Rhinacanthin C Alleviates Amyloid-β Fibrils’ Toxicity on Neurons and Attenuates Neuroinflammation Triggered by LPS, Amyloid-β, and Interferon-γ in Glial Cells

Figure 10

Schematic diagram showing the neuroprotective effect of RC via a mechanism involving NF-κB- and ERK-mediated signaling. LPS, Aβ, and IFN-γ initiate the inflammation by activating NF-κB and ERK pathways. The activation of NF-κB and ERK regulates the gene expression of proinflammatory mediators and neurotoxic factors that ultimately cause neurotoxicity. However, RC inhibits the NF-κB and ERK pathways to interfere with further inflammatory responses or neuronal damage.