Wogonin inhibits microglial cell migration via suppression of nuclear factor-kappa B activity

Previously, we and others have demonstrated that wogonin, an active component from the root of Scutellaria baicalensis Georgi, has a neuroprotective effect in cerebral ischemic insult. The neuroprotective effect of wogonin may at least in part be due to its anti-inflammatory properties. Microglial c...

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Veröffentlicht in:International immunopharmacology 2008-12, Vol.8 (12), p.1658-1662
Hauptverfasser: Piao, Hua Zi, Choi, In Young, Park, Jin-Sun, Kim, Hee-Sun, Cheong, Jae Hoon, Son, Kun Ho, Jeon, Su Jin, Ko, Kwang Ho, Kim, Won-Ki
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Sprache:eng
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Zusammenfassung:Previously, we and others have demonstrated that wogonin, an active component from the root of Scutellaria baicalensis Georgi, has a neuroprotective effect in cerebral ischemic insult. The neuroprotective effect of wogonin may at least in part be due to its anti-inflammatory properties. Microglial cells, well-known residential macrophages in the central nervous system, migrate to the ischemic lesion and play a pivotal role in the development of chronic inflammation. In the present study, we observed that wogonin potently inhibited microglial migration toward a chemokine, monocyte chemoattractant protein-1 (MCP-1). The anti-migratory effect of wogonin was provoked at nanomolar concentrations, at which wogonin did not significantly inhibit the production of cytokines and chemokines. NF-κB has previously shown to regulate microglial cell migration, and activation of cAMP-signaling pathway has also been associated with inhibition of microglial cell motility. In the present study, wogonin at low micromolar concentrations completely suppressed the activity of NF-κB in MCP-1-stimulated microglia, and NF-κB inhibitors such as N-acetyl cysteine and pyrrolidinedithiocarbamate inhibited the MCP-1-induced migration of microglial cells. However, wogonin did not stimulate the production of cAMP in microglial cells. Our results indicate that the anti-inflammatory activity of wogonin is exerted at least in part by suppressing microglial cell motility via inhibition of NF-κB activity.
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2008.07.018