참취로부터 분리된 Isoquercitrin의 항염증 및 뇌신경세포 보호 효과

초록

This study examined the anti-inflammatory and neuroprotective effects of isoquercitrin (Que) isolated from Aster scaber and its underlying mechanisms. Que inhibited the lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and tumor necrosis factor-α (TNF-α) in Raw264.7 macrophage cells, highlighting its anti-inflammatory activity. LPS activated the extracellular signal-regulated kinase (Erk) and p38 pathway and Que inhibited the phosphorylation of Erk and p38 (p-Erk and p-p38) in LPS-treated Raw264.7 macrophage cells. Sodium nitroprusside (SNP) was used as a NO donor. Que inhibited significantly the excessive production of NO in SNP-treated microglia and human brain neuroblastoma SK-N-SH cells. Que increased the level of SK-N-SH cell survival against toxicity by the excessive production of NO. These results suggest that Que has a neuroprotective effect in SNP-induced neuronal cell death and the neuroprotection may be correlated with its anti-inflammatory effect via the suppression of Erk and p38 signaling pathways in LPS-treated Raw264.7 macrophage cells. In addition, the downregulation of NO production may be a significant clinical value in developing strategies for the treatment of neurodegenerative diseases.

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