Gold drug auranofin could reduce neuroinflammation by inhibiting microglia cytotoxic secretions and primed respiratory burst

• We studied in vitro the anti-neuroinflammatory activity of several gold compounds.
• Auranofin reduced cytotoxic secretions by human microglia and microglia-like cells.
• Auranofin had a direct neuroprotective effect on SH-SY5Y neuronal cells.
• Auranofin inhibited primed respiratory burst of mononuclear phagocytes.
• At effective concentrations auranofin was not toxic.

Neuroinflammation contributes to the pathogenesis of neurological disorders. Anti-inflammatory treatments could potentially be used to slow down the progression of these diseases. We studied the anti-neuroinflammatory activity of gold compounds which have been used to treat rheumatoid arthritis. Non-toxic concentrations of auranofin (0.1–1 μM) significantly reduced the cytotoxic secretions by primary human microglia and microglia-like THP-1 promonocytic cells. Auranofin inhibited primed NADPH-oxidase dependent respiratory burst and secretion of tumor necrosis factor (TNF)-α and nitric oxide by monocytic cells. It had a direct neuroprotective effect on SH-SY5Y neuronal cells. Auranofin could have a novel application in the treatment of neurodegenerative diseases.