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미세아교세포의 염증반응에 미치는 청뇌명신환의 영향

Anti-inflammatory Effects of Cheongnoimyungshin-hwan in Microglia Cells

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Objectives: Activated microglia cells play an important role in inflammatory responses in the central nervous system (CNS) which are involved in neurodegenerative diseases. We attempted to determine the anti-inflammatory effects of Cheongnoimyungshin-hwan (CNMSH) in microglia cells. Methods: We examined the effect of CNMSH on the inflammatory responses in BV2 microglia cells induced by lipopolysaccharide (LPS) and explored the mechanism underlying the action of CNMSH. Results: BV2 cells treated with LPS showed an up-regulation of nitric oxide (NO), prostaglandin PGE2 (PGE2) and interleukin 1b (IL-1b) release, whereas CNMSH suppressed this up-regulation. CNMSH inhibited the induction of COX-2, iNOS and IL-1b proteins in LPS-treated BV2 cells and blocked the LPS-induced phosphorylation and nuclear translocation of nuclear factor kB (NF-kB). Furthermore, CNMSH attenuated the LPS-induced phosphorylation of extracellular signal-regulated kinase and p38 mitogen activated protein kinase (MAPK), as well as the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, but did not inhibit the LPS-induced phosphorylation of c-Jun amino terminal kinase. Conclusions: These results suggest that the inhibitory effect of CNMSH on the LPS-induced production of inflammatory mediators and cytokines in BV2 cells is associated with the suppression of the NF-kB and PI3KAkt signaling pathways.

Abstract

Objectives: Activated microglia cells play an important role in inflammatory responses in the central nervous system (CNS) which are involved in neurodegenerative diseases. We attempted to determine the anti-inflammatory effects of Cheongnoimyungshin-hwan (CNMSH) in microglia cells. Methods: We examined the effect of CNMSH on the inflammatory responses in BV2 microglia cells induced by lipopolysaccharide (LPS) and explored the mechanism underlying the action of CNMSH. Results: BV2 cells treated with LPS showed an up-regulation of nitric oxide (NO), prostaglandin PGE2 (PGE2) and interleukin 1b (IL-1b) release, whereas CNMSH suppressed this up-regulation. CNMSH inhibited the induction of COX-2, iNOS and IL-1b proteins in LPS-treated BV2 cells and blocked the LPS-induced phosphorylation and nuclear translocation of nuclear factor kB (NF-kB). Furthermore, CNMSH attenuated the LPS-induced phosphorylation of extracellular signal-regulated kinase and p38 mitogen activated protein kinase (MAPK), as well as the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, but did not inhibit the LPS-induced phosphorylation of c-Jun amino terminal kinase. Conclusions: These results suggest that the inhibitory effect of CNMSH on the LPS-induced production of inflammatory mediators and cytokines in BV2 cells is associated with the suppression of the NF-kB and PI3KAkt signaling pathways.

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