Microglia are activated in response to injury, infection, and toxic pro-inflammatory molecules that threaten neuronal survival. Long-term microglial activation plays a crucial role in the progression of neurodegenerative diseases, and negative regulators of this process have been recognized as potential therapeutic options for various neurological disorders. In this study, we evaluated the effects of Cyrtomium falcatum (L.f.) Presl (CFL) extracts on lipopolysaccharide (LPS)-induced activation of BV2 microglial cells. CFL extracts significantly reduced excessive nitric oxide production in LPS-stimulated BV2 cells and decreased the expression of inducible nitric oxide synthase, cyclooxygenase-2, and pro-inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) . Pretreatment with CFL extracts markedly suppressed the phosphorylation of mitogen-activated protein kinases (p38, JNK, and ERK1/2) and nuclear factor kappa B and modulated the antioxidant transcription factor, nuclear factor erythroid 2–related factor 2. In conclusion, these results indicate that CFL extracts exert neuroprotective effects by inhibiting pro-inflammatory signaling pathways and modulating antioxidant defense mechanisms, suggesting their potential as therapeutic candidates for neuroinflammatory disorders.
Choi et al. (Sun,) studied this question.