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Ameliorative effect of 1,8-cineole-rich Melaleuca citrina essential oil on LPSinduced inflammation and oxidative stress in RAW264.7 macrophages: experimental and computational studies
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DOI：10.1016/j.hermed.2025.101076.png)
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Abstract
En 中文
Introduction: Melaleuca citrina (Myrtaceae) is traditionally used to treat inflammation, digestive disorders, respiratory diseases, arthritis, pain, and infections. This study evaluated the effects of M. citrina essential oil (MCEO) on lipopolysaccharide-induced inflammation and oxidative stress in RAW264.7 macrophages using experimental and computational approaches. Methods: MCEO components were identified via GC-MS. Cytotoxicity by MTT assay in RAW264.7 cells determined an IC50 of MCEO as 26.89 mu g/mL. The effects of MCEO (6.5, 13, and 26 mu g/mL) and diclofenac on inflammatory mediators (COX, 5-LOX, MPO, iNOS, and NO) were assessed biochemically, whereas cytokines (IL-1 beta, IL-6, and TNF-alpha) were evaluated using ELISA. The antioxidant markers (SOD, CAT, GSH-Px, GSH, MDA, and total protein) were measured spectrophotometrically. ROS levels and mitochondrial membrane potential were analysed using DCFDA and flow cytometry, respectively. Molecular docking was performed to examine the interactions between major MCEO components and inflammatory markers. Results: MCEO reduced the viability of macrophages in a dose-dependent manner. At a concentration of 26 mu g/ mL, MCEO and diclofenac significantly decreased the levels of inflammatory mediators and cytokines. MCEO improved the antioxidant status by increasing the levels of SOD, CAT, GSH-Px, and total protein while reducing the MDA levels. MCEO also mitigated oxidative stress by lowering ROS and preserving mitochondrial membrane potential. Molecular docking confirmed strong interactions between the major MCEO components and inflammatory proteins, supporting the in vitro findings. Conclusion: MCEO effectively alleviated lipopolysaccharide-induced inflammation and oxidative stress, validating its traditional use in inflammatory conditions.
Keywords:
Cytotoxicity
Proinflammatory mediators
Proinflammatory cytokines
Reactive oxygen species
Mitochondrial membrane potential
Molecular docking
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1.9
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