Eriodictyol inhibits IL-1β-induced inflammatory response in human osteoarthritis chondrocytes
Copyright © 2018 Elsevier Masson SAS. All rights reserved..
Osteoarthritis (OA) is a degenerative disease of joints, which is closely associated with cartilage degradation. Eriodictyol, a natural flavonoid compound, has been reported to have anti-inflammatory and anti-osteoclastogenic effects. However, the effect of eriodictyol on inflammatory response in OA has not been investigated. Our results showed that eriodictyol attenuated the inhibition of cell viability in IL-1β-stimulated chondrocytes. In addition, eriodictyol inhibited the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and the production of prostaglandin E2 (PGE2) and nitric oxide (NO), which were induced by IL-1β. The induction of inflammatory cytokines and matrix metalloproteinases (MMPs) caused by IL-1β stimulation was also attenuated by eriodictyol. Furthermore, eriodictyol pretreatment inhibited IκBα degradation and the level of p-p65, and enhanced the up-regulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase 1 (HO-1) in IL-1β-stimulated chondrocytes. Si-Nrf2 treatment significantly inhibited the expressions of Nrf2 and HO-1 in chondrocytes. Additionally, si-Nrf2 transfection also abolished the anti-inflammatory effects of eriodictyol in chondrocytes. These findings indicated that eriodictyol exhibited anti-inflammatory effect in IL-1β-stimulated chondrocytes. The effect was mediated by inhibiting NF-κB via activating the Nrf2/HO-1 signaling pathway.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2018 |
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| Erschienen: |
2018 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:107 |
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| Enthalten in: |
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie - 107(2018) vom: 26. Nov., Seite 1128-1134 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wang, Yongsheng [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 03.01.2019 Date Revised 30.03.2022 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.biopha.2018.08.103 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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NLM288932919 |
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| 520 | |a Copyright © 2018 Elsevier Masson SAS. All rights reserved. | ||
| 520 | |a Osteoarthritis (OA) is a degenerative disease of joints, which is closely associated with cartilage degradation. Eriodictyol, a natural flavonoid compound, has been reported to have anti-inflammatory and anti-osteoclastogenic effects. However, the effect of eriodictyol on inflammatory response in OA has not been investigated. Our results showed that eriodictyol attenuated the inhibition of cell viability in IL-1β-stimulated chondrocytes. In addition, eriodictyol inhibited the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and the production of prostaglandin E2 (PGE2) and nitric oxide (NO), which were induced by IL-1β. The induction of inflammatory cytokines and matrix metalloproteinases (MMPs) caused by IL-1β stimulation was also attenuated by eriodictyol. Furthermore, eriodictyol pretreatment inhibited IκBα degradation and the level of p-p65, and enhanced the up-regulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase 1 (HO-1) in IL-1β-stimulated chondrocytes. Si-Nrf2 treatment significantly inhibited the expressions of Nrf2 and HO-1 in chondrocytes. Additionally, si-Nrf2 transfection also abolished the anti-inflammatory effects of eriodictyol in chondrocytes. These findings indicated that eriodictyol exhibited anti-inflammatory effect in IL-1β-stimulated chondrocytes. The effect was mediated by inhibiting NF-κB via activating the Nrf2/HO-1 signaling pathway | ||
| 650 | 4 | |a Journal Article | |
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| 700 | 1 | |a Shan, Xiaowei |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Guangjie |e verfasserin |4 aut | |
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