β-Caryophyllene downregualtes inflammatory cytokine expression and alleviates systemic inflammation in mice by inhibiting the NF-κB signaling pathway
Objective To investigate the anti-inflammatory mechanism of β-caryophyllene (BCP) on lipopolysaccharide (LPS)-induced systemic inflammation in mice. Methods C57BL mice were divided into control group, LPS-treated group, dexamethasone-treated group, and BCP-treated group. Twelve hours after the establishment of the whole body inflammation model by intraperitoneal injection of LPS, the serum levels of interleukin 1β(IL-1β), tumor necrosis factor α (TNF-α), and IL-6 were measured by ELISA. The protein levels of nuclear factor κB p65(NF-κB p65), myeloid differentiation primary response 88 (MyD88), and Toll-like receptor 4 (TLR4) in spleen tissue were assessed by Western blot analysis. ResultsCompared with the control group, the serum levels of the inflammatory cytokines IL-1β, TNF-α and IL-6 in the LPS-treated group were significantly increased. In addition, the pro-tein levels of NF-κB p65, MyD88 and TLR4 were increased in spleen tissues. Compared with the LPS-treated group, the protein levels of IL-1β, TNF-α and IL-6 in the BCP-treated group were decreased significantly. Furthermore, the protein levels of NF-κB p65, MyD88 and TLR4 in spleen tissue showed a remarkable reduction. The inhibitory effect was notably better in the 3.5 μg/(L.d) BCP-treated group than in the 3 μg/(L.d) BCP-treated group. Conclusion BCP exerts anti-inflammatory effects by downregulating inflammatory cytokine expression through the inhibition of the NF-κB signaling pathway.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:40 |
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| Enthalten in: |
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology - 40(2024), 3 vom: 21. März, Seite 229-234 |
| Sprache: |
Chinesisch |
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| Beteiligte Personen: |
Yang, Bingye [VerfasserIn] |
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| Anmerkungen: |
Date Completed 22.03.2024 Date Revised 22.03.2024 published: Print Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM370016157 |
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| 100 | 1 | |a Yang, Bingye |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a β-Caryophyllene downregualtes inflammatory cytokine expression and alleviates systemic inflammation in mice by inhibiting the NF-κB signaling pathway |
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| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Objective To investigate the anti-inflammatory mechanism of β-caryophyllene (BCP) on lipopolysaccharide (LPS)-induced systemic inflammation in mice. Methods C57BL mice were divided into control group, LPS-treated group, dexamethasone-treated group, and BCP-treated group. Twelve hours after the establishment of the whole body inflammation model by intraperitoneal injection of LPS, the serum levels of interleukin 1β(IL-1β), tumor necrosis factor α (TNF-α), and IL-6 were measured by ELISA. The protein levels of nuclear factor κB p65(NF-κB p65), myeloid differentiation primary response 88 (MyD88), and Toll-like receptor 4 (TLR4) in spleen tissue were assessed by Western blot analysis. ResultsCompared with the control group, the serum levels of the inflammatory cytokines IL-1β, TNF-α and IL-6 in the LPS-treated group were significantly increased. In addition, the pro-tein levels of NF-κB p65, MyD88 and TLR4 were increased in spleen tissues. Compared with the LPS-treated group, the protein levels of IL-1β, TNF-α and IL-6 in the BCP-treated group were decreased significantly. Furthermore, the protein levels of NF-κB p65, MyD88 and TLR4 in spleen tissue showed a remarkable reduction. The inhibitory effect was notably better in the 3.5 μg/(L.d) BCP-treated group than in the 3 μg/(L.d) BCP-treated group. Conclusion BCP exerts anti-inflammatory effects by downregulating inflammatory cytokine expression through the inhibition of the NF-κB signaling pathway | ||
| 650 | 4 | |a English Abstract | |
| 650 | 4 | |a Journal Article | |
| 650 | 7 | |a NF-kappa B |2 NLM | |
| 650 | 7 | |a caryophyllene |2 NLM | |
| 650 | 7 | |a BHW853AU9H |2 NLM | |
| 650 | 7 | |a Toll-Like Receptor 4 |2 NLM | |
| 650 | 7 | |a Cytokines |2 NLM | |
| 650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
| 650 | 7 | |a Interleukin-6 |2 NLM | |
| 650 | 7 | |a Lipopolysaccharides |2 NLM | |
| 650 | 7 | |a Myeloid Differentiation Factor 88 |2 NLM | |
| 650 | 7 | |a Adaptor Proteins, Signal Transducing |2 NLM | |
| 650 | 7 | |a Interleukin-1beta |2 NLM | |
| 650 | 7 | |a Anti-Inflammatory Agents |2 NLM | |
| 650 | 7 | |a Polycyclic Sesquiterpenes |2 NLM | |
| 700 | 1 | |a Wang, Minlong |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Ying |e verfasserin |4 aut | |
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