Modulation of BV-2 microglia functions by novel quercetin pivaloyl ester.

摘要: Chronic inflammation in brain plays a critical role major neurodegenerative diseases such as Alzheimer's, Parkinson's disease, stroke or multiple sclerosis. Microglia, resident macrophages and intristinc components of CNS, appear to be main effectors this pathological process. Quercetin, naturally occurring flavonoid, was proven downregulate inflammatory genes microglia. Synthetically modified quercetin, 3′-O-(3-chloropivaloyl) quercetin (CPQ), is assumed possess better biological availability enhanced antioxidant properties. In the present study, antineuroinflammatory capability novel compound CPQ assessed BV-2 microglial cells. Our data show that treatment with attenuated production mediators, nitric oxide (NO) tumour necrosis factor-α (TNF-α), LPS-stimulated microglia somewhat more efficiently than did (p > 0.05 for vs. quercetin-treated group). Also, protein level inducible NO synthase (iNOS) LPS-activated some extent effectively supressed by unmodified flavonoid. In consistence their effects on pro-inflammatory markers, showed down-regulation NFκB activation. This analogue caused also decline proliferation interfering cell cycle progression (p < 0.001 However, not remarkably affect viability. addition, minor suppression PMA-induced generation superoxide quercetin. Neither nor influenced phagocytosis cells. These results point therapeutic potential 3′-O-(3-chloropivaloyl)quercetin (CPQ) antiinflammatory drug diseases, mediating favourable modulation functions