Linalool and linalyl acetate attenuated canonical pathway of NF-κB signaling in HepG2 cells
Background and Aims Lavender oil is often used in aromatherapy due to its anti-inflammatory therapeutic potential. The anti-inflammatory effect through NF-κB signaling has not been well characterized. In this study, we investigated these effects using the HepG2 liver cell line. Methods Two major com...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2025-12-01
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| Series: | All Life |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/26895293.2025.2527624 |
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| Summary: | Background and Aims Lavender oil is often used in aromatherapy due to its anti-inflammatory therapeutic potential. The anti-inflammatory effect through NF-κB signaling has not been well characterized. In this study, we investigated these effects using the HepG2 liver cell line. Methods Two major components of lavender oil, Linalool and Linalyl acetate (LA), were used in HepG2 cell line. Lipopolysaccharide (LPS) was used to induce inflammation. NF-κB signaling was examined using Western blotting and confocal microscopy, while interleukin-6 (IL-6) expression was analyzed by quantitative PCR. Results LPS up-regulated NF-κB expression by P65 phosphorylation, and IκBα phosphorylation, but could not be induced by Linalool or LA. Linalool and LA both down-regulated P65, IκBα phosphorylation, and IL-6 expression in HepG2 cells. The down-regulation effect of Linalool and LA on LPS-induced P65, and IκBα phosphorylation was demonstrated by confocal microscopy and electrophoretic mobility-shift assays. Conclusions Linalool and LA significantly down regulated NF-κB signaling in HepG2 cells. They effectively inhibited LPS-induced NF-κB activation by suppressing p65 expression and preventing IκBα degradation, demonstrating potent anti-inflammatory effects via the canonical pathway. Further investigation remains warranted to explore the broader anti-inflammatory potential of lavender oil in vivo and in humans. |
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| ISSN: | 2689-5307 |