Exopolysaccharide of Laetiporus sulphureus var. miniatus downregulates LPS-induced production of NO, PGE₂, and TNF-¦Á in BV2 microglia cells via suppression of the NF-¦ÊB pathway

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• 作者：R.G.P.T. Jayasooriya^a ;   ; ¹ ; Chang-Hee Kang^a ;   ; ¹ ; Min-Jeong Seo^b ;   ; ¹ ; Yung Hyun Choi^c ; Yong-Kee Jeong^b ;   ; ^{ykj9912@dau.ac.kr} ; Gi-Young Kim^a ;   ; ^{immunkim@jejunu.ac.kr}
• 关键词：Exopolysaccharide ; Inducible nitric oxide synthase ; Cyclooxygenase-2 ; Tumor necrosis factor-¦Á ; Lipopolysaccharide ; Nuclear factor-¦ÊB
• 刊名：Food and Chemical Toxicology
• 出版年：2011
• 出版时间：November 2011
• 年：2011
• 卷：49
• 期：11
• 页码：2758-2764
• 全文大小：584 K

文摘

Our previous study showed that the exopolysaccharide (EPS) of mlns="""">Laetiporus sulphureus var. mlns="""">miniatus was well characterized and prevented cell damage in streptozotocin-induced apoptosismlns="""">. However, little is known about the molecular mechanisms underlying its anti-inflammatory effects. Therefore, we attempted in this study to determine whether EPS induces a significant inhibition of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine BV2 microglia cells. Our results showed that EPS significantly inhibited LPS-induced pro-inflammatory mediators, such as nitric oxide (NO), prostaglandin E_mlns="""">2 (PGE_mlns="""">2), and tumor necrosis factor-¦Á (TNF-¦Á), without any significant cytotoxicity. EPS also downregulated mRNA and protein expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-¦Á in LPS-induced BV2 microglia cells. Our data also revealed that EPS treatment significantly reduced translocation of nuclear factor-¦ÊB (NF-¦ÊB) subunit p65 and its DNA-binding activity in LPS-stimulated BV2 microglia cells. Furthermore, we confirmed by using proteasome inhibitor mlns="""">N-acetyl-l-cysteine (NAC), that the inhibition of NF-¦ÊB activity influenced the expression of pro-inflammatory genes in LPS-induced BV2 microglia cells. As expected, NAC suppressed the expression of iNOS, COX-2, and TNF-¦Á by blocking proteasome-mediated degradation. Taken together, our data indicate that EPS inhibits the expression of pro-inflammatory mediators by suppressing NF-¦ÊB activity.