Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury
Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to inve...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Zhongyuan [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021transfer abstract |
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| Schlagwörter: |
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| Umfang: |
13 |
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| Übergeordnetes Werk: |
Enthalten in: New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells - Wu, Zhi-Sheng ELSEVIER, 2020, the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research, New York, NY [u.a.] |
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| Übergeordnetes Werk: |
volume:168 ; year:2021 ; day:20 ; month:05 ; pages:142-154 ; extent:13 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.freeradbiomed.2021.03.037 |
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ELV053746112 |
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| 245 | 1 | 0 | |a Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury |
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| 520 | |a Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. | ||
| 520 | |a Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. | ||
| 650 | 7 | |a Reactive oxygen species |2 Elsevier | |
| 650 | 7 | |a Kaempferol |2 Elsevier | |
| 650 | 7 | |a MAPKs–NF–κB signaling pathway |2 Elsevier | |
| 650 | 7 | |a NLRP3-Mediated pyroptosis |2 Elsevier | |
| 650 | 7 | |a Neuroinflammation |2 Elsevier | |
| 700 | 1 | |a Yao, Xinqiang |4 oth | |
| 700 | 1 | |a Sun, Baihui |4 oth | |
| 700 | 1 | |a Jiang, Wangsheng |4 oth | |
| 700 | 1 | |a Liao, Congrui |4 oth | |
| 700 | 1 | |a Dai, Xiangheng |4 oth | |
| 700 | 1 | |a Chen, Yu |4 oth | |
| 700 | 1 | |a Chen, Jianting |4 oth | |
| 700 | 1 | |a Ding, Ruoting |4 oth | |
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10.1016/j.freeradbiomed.2021.03.037 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001997.pica (DE-627)ELV053746112 (ELSEVIER)S0891-5849(21)00197-0 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Liu, Zhongyuan verfasserin aut Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury 2021transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Reactive oxygen species Elsevier Kaempferol Elsevier MAPKs–NF–κB signaling pathway Elsevier NLRP3-Mediated pyroptosis Elsevier Neuroinflammation Elsevier Yao, Xinqiang oth Sun, Baihui oth Jiang, Wangsheng oth Liao, Congrui oth Dai, Xiangheng oth Chen, Yu oth Chen, Jianting oth Ding, Ruoting oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:168 year:2021 day:20 month:05 pages:142-154 extent:13 https://doi.org/10.1016/j.freeradbiomed.2021.03.037 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 168 2021 20 0520 142-154 13 |
| spelling |
10.1016/j.freeradbiomed.2021.03.037 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001997.pica (DE-627)ELV053746112 (ELSEVIER)S0891-5849(21)00197-0 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Liu, Zhongyuan verfasserin aut Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury 2021transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Reactive oxygen species Elsevier Kaempferol Elsevier MAPKs–NF–κB signaling pathway Elsevier NLRP3-Mediated pyroptosis Elsevier Neuroinflammation Elsevier Yao, Xinqiang oth Sun, Baihui oth Jiang, Wangsheng oth Liao, Congrui oth Dai, Xiangheng oth Chen, Yu oth Chen, Jianting oth Ding, Ruoting oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:168 year:2021 day:20 month:05 pages:142-154 extent:13 https://doi.org/10.1016/j.freeradbiomed.2021.03.037 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 168 2021 20 0520 142-154 13 |
| allfields_unstemmed |
10.1016/j.freeradbiomed.2021.03.037 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001997.pica (DE-627)ELV053746112 (ELSEVIER)S0891-5849(21)00197-0 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Liu, Zhongyuan verfasserin aut Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury 2021transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Reactive oxygen species Elsevier Kaempferol Elsevier MAPKs–NF–κB signaling pathway Elsevier NLRP3-Mediated pyroptosis Elsevier Neuroinflammation Elsevier Yao, Xinqiang oth Sun, Baihui oth Jiang, Wangsheng oth Liao, Congrui oth Dai, Xiangheng oth Chen, Yu oth Chen, Jianting oth Ding, Ruoting oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:168 year:2021 day:20 month:05 pages:142-154 extent:13 https://doi.org/10.1016/j.freeradbiomed.2021.03.037 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 168 2021 20 0520 142-154 13 |
| allfieldsGer |
10.1016/j.freeradbiomed.2021.03.037 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001997.pica (DE-627)ELV053746112 (ELSEVIER)S0891-5849(21)00197-0 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Liu, Zhongyuan verfasserin aut Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury 2021transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Reactive oxygen species Elsevier Kaempferol Elsevier MAPKs–NF–κB signaling pathway Elsevier NLRP3-Mediated pyroptosis Elsevier Neuroinflammation Elsevier Yao, Xinqiang oth Sun, Baihui oth Jiang, Wangsheng oth Liao, Congrui oth Dai, Xiangheng oth Chen, Yu oth Chen, Jianting oth Ding, Ruoting oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:168 year:2021 day:20 month:05 pages:142-154 extent:13 https://doi.org/10.1016/j.freeradbiomed.2021.03.037 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 168 2021 20 0520 142-154 13 |
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10.1016/j.freeradbiomed.2021.03.037 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001997.pica (DE-627)ELV053746112 (ELSEVIER)S0891-5849(21)00197-0 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Liu, Zhongyuan verfasserin aut Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury 2021transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. Reactive oxygen species Elsevier Kaempferol Elsevier MAPKs–NF–κB signaling pathway Elsevier NLRP3-Mediated pyroptosis Elsevier Neuroinflammation Elsevier Yao, Xinqiang oth Sun, Baihui oth Jiang, Wangsheng oth Liao, Congrui oth Dai, Xiangheng oth Chen, Yu oth Chen, Jianting oth Ding, Ruoting oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:168 year:2021 day:20 month:05 pages:142-154 extent:13 https://doi.org/10.1016/j.freeradbiomed.2021.03.037 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 168 2021 20 0520 142-154 13 |
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Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury |
| abstract |
Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. |
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Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. |
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Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI. |
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10.1016/j.freeradbiomed.2021.03.037 |
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2024-07-06T19:48:05.101Z |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV053746112</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626035302.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">210910s2021 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.freeradbiomed.2021.03.037</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001997.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV053746112</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0891-5849(21)00197-0</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">620</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">52.57</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">53.36</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Liu, Zhongyuan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Pretreatment with kaempferol attenuates microglia-mediate neuroinflammation by inhibiting MAPKs–NF–κB signaling pathway and pyroptosis after secondary spinal cord injury</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">13</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. A combination of molecular and histological methods was used to clarify the mechanism and explore the signaling pathway both in vivo and in vitro. One-way analysis of variance (ANOVA) was conducted with Bonferroni post hoc tests to examine the differences between groups. The in vivo studies showed that kaempferol could improve the recovery of hindlimb motor function and ameliorate tissue damage in the spinal cord after SCI. Moreover, administration of kaempferol reduced microglia activation and oxidative stress level in the spinal cord. The in vitro studies showed that kaempferol suppressed the microglia activation resulting from the administration of LPS with ATP to BV-2 cells. Pretreated BV2 cells with kaempferol reduced the generation of reactive oxygen species (ROS) by inhibiting NADPH oxidase 4, and then, suppressed the phosphorylation of p38 MAPK and JNK, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. We also observed that kaempferol could inhibite the pyroptosis related proteins (NLRP3 Caspase-1 p10 ASC N-GSDMD) and reduce the release of IL-18 and IL-1β. In conclusion, kaempferol was able to reduce oxidative stress and inflammatory response through down-regulation of ROS dependent MAPKs- NF-κB and pyroptosis signaling pathway, which suggested that kaempferol might be a novel promising therapeutic agent for SCI.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Spinal cord injury (SCI) is a devastating injury that characterized by oxidative stress and inflammatory response. Kaempferol is reported to be an anti-neuroinflammation in neurologic disorders. Nevertheless, the role and mechanism of kaempferol in SCI remains unclear. The present study aims to investigate effects of kaempferol on SCI and its possible underlying mechanisms in in vivo and in vitro models. A C5 hemi-contusion injury was induced in Sprague-Dawley rats to investigate the neuroprotective effects of kaempferol after SCI. For in vitro study, the BV2 microglia cell lines were pretreated with or without kaempferol. 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