A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis
The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1...
Ausführliche Beschreibung
Autor*in: |
Gu, Chunping [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2014transfer abstract |
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Schlagwörter: |
Leupeptin (Pubchem CID: 72429) Lipopolysaccharide (Pubchem CID: 11970143) Aprotinin (Pubchem CID: 16130295) Pepstatin (Pubchem CID: 5478883) |
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Umfang: |
8 |
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Übergeordnetes Werk: |
Enthalten in: Mexican student-teachers’ “English” language praxicum: Decolonizing attempts - López-Gopar, Mario E. ELSEVIER, 2022, EJP, New York, NY [u.a.] |
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Übergeordnetes Werk: |
volume:729 ; year:2014 ; day:15 ; month:04 ; pages:22-29 ; extent:8 |
Links: |
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DOI / URN: |
10.1016/j.ejphar.2014.01.019 |
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Katalog-ID: |
ELV023064870 |
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245 | 1 | 0 | |a A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis |
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520 | |a The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. | ||
520 | |a The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. | ||
650 | 7 | |a Leupeptin (Pubchem CID: 72429) |2 Elsevier | |
650 | 7 | |a Lipopolysaccharide (Pubchem CID: 11970143) |2 Elsevier | |
650 | 7 | |a G418 (Pubchem CID: 123865) |2 Elsevier | |
650 | 7 | |a PMSF (Pubchem CID: 4784) |2 Elsevier | |
650 | 7 | |a Aprotinin (Pubchem CID: 16130295) |2 Elsevier | |
650 | 7 | |a Pepstatin (Pubchem CID: 5478883) |2 Elsevier | |
650 | 7 | |a DAPI (Pubchem CID: 2954) |2 Elsevier | |
650 | 7 | |a BAY 11-7082 (Pubchem CID: 5353431) |2 Elsevier | |
650 | 7 | |a MTT (Pubchem CID: 64965) |2 Elsevier | |
650 | 7 | |a Sodium fluoride (Pubchem CID: 5235) |2 Elsevier | |
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700 | 1 | |a Yu, Le |4 oth | |
700 | 1 | |a He, Xiao-Yang |4 oth | |
700 | 1 | |a Zhong, Desheng |4 oth | |
700 | 1 | |a He, Longgang |4 oth | |
700 | 1 | |a Lv, Longyun |4 oth | |
700 | 1 | |a Xie, Lan |4 oth | |
700 | 1 | |a Liu, Shuwen |4 oth | |
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10.1016/j.ejphar.2014.01.019 doi GBVA2014020000026.pica (DE-627)ELV023064870 (ELSEVIER)S0014-2999(14)00020-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Gu, Chunping verfasserin aut A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis 2014transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. Leupeptin (Pubchem CID: 72429) Elsevier Lipopolysaccharide (Pubchem CID: 11970143) Elsevier G418 (Pubchem CID: 123865) Elsevier PMSF (Pubchem CID: 4784) Elsevier Aprotinin (Pubchem CID: 16130295) Elsevier Pepstatin (Pubchem CID: 5478883) Elsevier DAPI (Pubchem CID: 2954) Elsevier BAY 11-7082 (Pubchem CID: 5353431) Elsevier MTT (Pubchem CID: 64965) Elsevier Sodium fluoride (Pubchem CID: 5235) Elsevier Yu, Fang-Lin oth Yu, Le oth He, Xiao-Yang oth Zhong, Desheng oth He, Longgang oth Lv, Longyun oth Xie, Lan oth Liu, Shuwen oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:729 year:2014 day:15 month:04 pages:22-29 extent:8 https://doi.org/10.1016/j.ejphar.2014.01.019 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 729 2014 15 0415 22-29 8 045F 610 |
spelling |
10.1016/j.ejphar.2014.01.019 doi GBVA2014020000026.pica (DE-627)ELV023064870 (ELSEVIER)S0014-2999(14)00020-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Gu, Chunping verfasserin aut A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis 2014transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. Leupeptin (Pubchem CID: 72429) Elsevier Lipopolysaccharide (Pubchem CID: 11970143) Elsevier G418 (Pubchem CID: 123865) Elsevier PMSF (Pubchem CID: 4784) Elsevier Aprotinin (Pubchem CID: 16130295) Elsevier Pepstatin (Pubchem CID: 5478883) Elsevier DAPI (Pubchem CID: 2954) Elsevier BAY 11-7082 (Pubchem CID: 5353431) Elsevier MTT (Pubchem CID: 64965) Elsevier Sodium fluoride (Pubchem CID: 5235) Elsevier Yu, Fang-Lin oth Yu, Le oth He, Xiao-Yang oth Zhong, Desheng oth He, Longgang oth Lv, Longyun oth Xie, Lan oth Liu, Shuwen oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:729 year:2014 day:15 month:04 pages:22-29 extent:8 https://doi.org/10.1016/j.ejphar.2014.01.019 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 729 2014 15 0415 22-29 8 045F 610 |
allfields_unstemmed |
10.1016/j.ejphar.2014.01.019 doi GBVA2014020000026.pica (DE-627)ELV023064870 (ELSEVIER)S0014-2999(14)00020-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Gu, Chunping verfasserin aut A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis 2014transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. Leupeptin (Pubchem CID: 72429) Elsevier Lipopolysaccharide (Pubchem CID: 11970143) Elsevier G418 (Pubchem CID: 123865) Elsevier PMSF (Pubchem CID: 4784) Elsevier Aprotinin (Pubchem CID: 16130295) Elsevier Pepstatin (Pubchem CID: 5478883) Elsevier DAPI (Pubchem CID: 2954) Elsevier BAY 11-7082 (Pubchem CID: 5353431) Elsevier MTT (Pubchem CID: 64965) Elsevier Sodium fluoride (Pubchem CID: 5235) Elsevier Yu, Fang-Lin oth Yu, Le oth He, Xiao-Yang oth Zhong, Desheng oth He, Longgang oth Lv, Longyun oth Xie, Lan oth Liu, Shuwen oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:729 year:2014 day:15 month:04 pages:22-29 extent:8 https://doi.org/10.1016/j.ejphar.2014.01.019 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 729 2014 15 0415 22-29 8 045F 610 |
allfieldsGer |
10.1016/j.ejphar.2014.01.019 doi GBVA2014020000026.pica (DE-627)ELV023064870 (ELSEVIER)S0014-2999(14)00020-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Gu, Chunping verfasserin aut A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis 2014transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. Leupeptin (Pubchem CID: 72429) Elsevier Lipopolysaccharide (Pubchem CID: 11970143) Elsevier G418 (Pubchem CID: 123865) Elsevier PMSF (Pubchem CID: 4784) Elsevier Aprotinin (Pubchem CID: 16130295) Elsevier Pepstatin (Pubchem CID: 5478883) Elsevier DAPI (Pubchem CID: 2954) Elsevier BAY 11-7082 (Pubchem CID: 5353431) Elsevier MTT (Pubchem CID: 64965) Elsevier Sodium fluoride (Pubchem CID: 5235) Elsevier Yu, Fang-Lin oth Yu, Le oth He, Xiao-Yang oth Zhong, Desheng oth He, Longgang oth Lv, Longyun oth Xie, Lan oth Liu, Shuwen oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:729 year:2014 day:15 month:04 pages:22-29 extent:8 https://doi.org/10.1016/j.ejphar.2014.01.019 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 729 2014 15 0415 22-29 8 045F 610 |
allfieldsSound |
10.1016/j.ejphar.2014.01.019 doi GBVA2014020000026.pica (DE-627)ELV023064870 (ELSEVIER)S0014-2999(14)00020-X DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Gu, Chunping verfasserin aut A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis 2014transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. Leupeptin (Pubchem CID: 72429) Elsevier Lipopolysaccharide (Pubchem CID: 11970143) Elsevier G418 (Pubchem CID: 123865) Elsevier PMSF (Pubchem CID: 4784) Elsevier Aprotinin (Pubchem CID: 16130295) Elsevier Pepstatin (Pubchem CID: 5478883) Elsevier DAPI (Pubchem CID: 2954) Elsevier BAY 11-7082 (Pubchem CID: 5353431) Elsevier MTT (Pubchem CID: 64965) Elsevier Sodium fluoride (Pubchem CID: 5235) Elsevier Yu, Fang-Lin oth Yu, Le oth He, Xiao-Yang oth Zhong, Desheng oth He, Longgang oth Lv, Longyun oth Xie, Lan oth Liu, Shuwen oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:729 year:2014 day:15 month:04 pages:22-29 extent:8 https://doi.org/10.1016/j.ejphar.2014.01.019 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 729 2014 15 0415 22-29 8 045F 610 |
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610 610 DE-600 370 VZ 5,3 ssgn A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis Leupeptin (Pubchem CID: 72429) Elsevier Lipopolysaccharide (Pubchem CID: 11970143) Elsevier G418 (Pubchem CID: 123865) Elsevier PMSF (Pubchem CID: 4784) Elsevier Aprotinin (Pubchem CID: 16130295) Elsevier Pepstatin (Pubchem CID: 5478883) Elsevier DAPI (Pubchem CID: 2954) Elsevier BAY 11-7082 (Pubchem CID: 5353431) Elsevier MTT (Pubchem CID: 64965) Elsevier Sodium fluoride (Pubchem CID: 5235) Elsevier |
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A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis |
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A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis |
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a novel synthetic dibenzocyclooctadiene lignan analog xlyf-104-6 attenuates lipopolysaccharide-induced inflammatory response in raw264.7 macrophage cells and protects balb/c mice from sepsis |
title_auth |
A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis |
abstract |
The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. |
abstractGer |
The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. |
abstract_unstemmed |
The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug. |
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title_short |
A novel synthetic dibenzocyclooctadiene lignan analog XLYF-104-6 attenuates lipopolysaccharide-induced inflammatory response in RAW264.7 macrophage cells and protects BALB/c mice from sepsis |
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These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The wide range of inflammation mechanisms under control by NF-κB makes this pathway as an attractive target for new anti-inflammatory drugs. Herein, we showed that a new dibenzocyclooctadiene lignan analog XLYF-104-6, with a chemical name of 1,2,3,10,11-pentamethoxydibenzocycloocta-6,7-[c] pyrrole-1,3-dione, inhibited lipopolysaccharide (LPS)-induced NF-κB activation in RAW264.7 cells through preventing IκBα degradation and p65 nuclear translocation. The inhibitory activity of this compound on NF-κB activation contributes to the reduction of LPS-induced TNF-α and IL-6 productions. Notably, XLYF-104-6 suppressed LPS-induced iNOS expression and NO production in a NF-κB independent manner, since IKK inhibitor BAY 11-7082 has failed to exert similar inhibitory effect on iNOS expression and NO production. In addition, XLFY-104-6 also exerted anti-inflammatory action in endotoxemic mice by decreasing plasma LPS-induced TNF-α and IL-1β levels as well as increasing plasma LPS-induced IL-10 concentrations. These findings suggest XLYF-104-6 could act as a leading compound for developing a potential anti-inflammatory drug.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Leupeptin (Pubchem CID: 72429)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Lipopolysaccharide (Pubchem CID: 11970143)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">G418 (Pubchem CID: 123865)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PMSF (Pubchem CID: 4784)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Aprotinin (Pubchem CID: 16130295)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Pepstatin (Pubchem CID: 5478883)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">DAPI (Pubchem CID: 2954)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">BAY 11-7082 (Pubchem CID: 5353431)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MTT (Pubchem CID: 64965)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Sodium fluoride (Pubchem CID: 5235)</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yu, Fang-Lin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yu, Le</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Xiao-Yang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhong, Desheng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Longgang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lv, Longyun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xie, Lan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Shuwen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">López-Gopar, Mario E. ELSEVIER</subfield><subfield code="t">Mexican student-teachers’ “English” language praxicum: Decolonizing attempts</subfield><subfield code="d">2022</subfield><subfield code="d">EJP</subfield><subfield code="g">New York, NY [u.a.]</subfield><subfield code="w">(DE-627)ELV008405875</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:729</subfield><subfield code="g">year:2014</subfield><subfield code="g">day:15</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:22-29</subfield><subfield code="g">extent:8</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.ejphar.2014.01.019</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">729</subfield><subfield code="j">2014</subfield><subfield code="b">15</subfield><subfield code="c">0415</subfield><subfield code="h">22-29</subfield><subfield code="g">8</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
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