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Theissenolactone C is a **fungal-derived small molecule polyketide** originally isolated from *Theissenia cinerea*. It exhibits significant **anti-inflammatory and neuroprotective effects**, particularly in models of ocular and neuroinflammation. In experimental studies, theissenolactone C (LC53) has been shown to attenuate endotoxin-induced uveitis in rats by inhibiting **ocular inflammatory responses, glial activation, and apoptosis**. Mechanistically, it reduces pro-inflammatory cytokines (such as TNF-α), chemokines, protein leakage, and matrix metalloproteinase activity. It decreases oxidative stress and suppresses microglial activation by inhibiting the NF-κB signaling pathway and mitogen-activated protein kinase (MAPK) pathways (notably JNK and ERK). In vitro, LC53 inhibits nitric oxide, prostaglandin E2, reactive oxygen species, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) production in LPS-stimulated microglial cells. The compound has demonstrated **potent nitric oxide inhibitory activity** (IC50 ≈ 1.1 µM) in microglial BV2 cells and has not shown significant cytotoxic effects at effective concentrations. While currently not approved as a pharmaceutical, theissenolactone C is being studied for the **treatment of uveitis and retinal inflammatory diseases**, with potential broader implications for neuroinflammation and related disorders[5][6][8].
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