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   <subfield code="a">10.1007/s00011-011-0345-2</subfield>
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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s00011-011-0345-2</subfield>
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   <subfield code="a">Methyl-1-hydroxy-2-naphthoate, a novel naphthol derivative, inhibits lipopolysaccharide-induced inflammatory response in macrophages via suppression of NF-κB, JNK and p38 MAPK pathways</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Jun-Yan Zhang, Hong Jin, Guang-Fa Wang, Peng-Jiu Yu, Shao-Yu Wu, Zheng-Guang Zhu, Zhong-Huang Li, Yuan-Xin Tian, Wei Xu, Jia-Jie Zhang, Shu-Guang Wu]</subfield>
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   <subfield code="a">Objective and design: The anti-inflammatory effect of methyl-1-hydroxy-2-naphthoate (MHNA), a novel naphthol derivative, was evaluated in the lipopolysaccharide (LPS)-induced inflammatory response in murine macrophages. Materials and methods: The release of nitric oxide (NO), interleukin-1beta (IL-1β) and interleukin-6 (IL-6) were detected by the Griess reagent and ELISA methods. The protein expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) were examined by Western blotting. The mRNA expressions of IL-1β, IL-6, iNOS and COX-2 were determined by real-time PCR. Activation of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) pathways were detected by Western blotting, reporter gene assay and electrophoretic mobility shift assay. Results: MHNA significantly inhibited the release of NO, IL-1β and IL-6 as well as the protein expression of iNOS and COX-2 in LPS-stimulated macrophages. It also inhibited the mRNA expression of iNOS, COX-2, IL-1β and IL-6. Further studies indicated that MHNA inhibited LPS-induced increases in NF-κB DNA-binding activity and NF-κB transcriptional activity as well as IκB-α degradation and NF-κB translocation in a dose-dependent manner. Meanwhile, the activation of p38 MAPK and c-Jun N-terminal kinases (JNK) induced by LPS were decreased by MHNA. Conclusions: MHNA inhibits the LPS-induced inflammatory response in murine macrophages via suppression of NF-κB and MAPKs signaling pathways activation.</subfield>
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   <subfield code="a">Methyl-1-hydroxy-2-naphthoate</subfield>
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   <subfield code="a">Macrophage</subfield>
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   <subfield code="a">COX-2 : Cyclooxygenase-2</subfield>
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   <subfield code="a">EMSA : Electrophoretic mobility shift assay</subfield>
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   <subfield code="a">ERK : Extracellular signal-regulated kinases</subfield>
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   <subfield code="a">iNOS : Inducible nitric oxide synthase</subfield>
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   <subfield code="a">LPS : Lipopolysaccharide</subfield>
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   <subfield code="a">NO : Nitric oxide</subfield>
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   <subfield code="a">NF-κB : Nuclear factor kappa B</subfield>
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   <subfield code="a">PGE2 : Prostaglandin E2</subfield>
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   <subfield code="a">TNF-α : Tumor necrosis factor alpha</subfield>
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   <subfield code="D">Jun-Yan</subfield>
   <subfield code="u">School of Pharmaceutical Sciences, Southern Medical University, 510515, Guangzhou, China</subfield>
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