ArticleBiochemistry and biophysics reports2026
10,11-Dehydrocurvularin attenuates LPS-induced neuroinflammation in BV2 cells by inhibiting the TLR2/MyD88/NLRP3 signaling pathway.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neuroinflammation, driven by microglial activation and Toll-like receptor 2 (TLR2) signaling, is a hallmark of neurodegenerative diseases. While 10,11-Dehydrocurvularin (DCV) is known for its anti-inflammatory properties, its specific effects on neuroinflammation remain poorly understood. This study evaluated DCV in lipopolysaccharide (LPS)-stimulated BV2 microglia. Nitric oxide (NO) was measured via the Griess assay, interleukin-1β (IL-1β) and IL-6 levels were quantified using ELISA or RT-qPCR, and the TLR2/MyD88/NLRP3 pathway was analyzed via Western blotting. To validate the target specificity, we employed a TLR2 agonist (Pam3CSK4), a pharmacological inhibitor (C29), and siRNA-mediated knockdown. Results showed that DCV concentration-dependently inhibited LPS-induced NO production (IC
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