Anti-inflammatory Effect of Essential Oil from Citrus aurantium L. var. amara Engl.
Chun-Yan ShenJian-Guo JiangWei ZhuQin Ou-YangPublished in: Journal of agricultural and food chemistry (2017)
Essential oil has been popularly used as an alternative for the treatment of inflammation. The bioactivities of essential oil from blossoms of Citrus aurantium L. var. amara Engl (CAVAO) showed greater anti-inflammation potential than that of antioxidant, anticancer, and 3T3-L1 proliferation inhibition. CAVAO (250 μg/mL) significantly inhibited production of nitric oxide (NO) (99.54 ± 2.81%), interleukin-6 (IL-6) (98.11 ± 1.62%), tumor necrosis factor-α (TNF-α) (41.84 ± 1.52%), and interleukin-1β (IL-1β) (56.09 ± 2.21%) as well as their gene expression level. CAVAO also markedly decreased the expression levels of cyclooxygenase-2 (COX-2) gene and protein. Furthermore, CAVAO inhibited nuclear factor-κB (NF-κB) activation, which was justified by the inhibitory effect on NF-κB nuclear translocation, IκBα phosphorylation and degradation, and phosphorylation-dependent IκB kinase activation in RAW264.7 cells stimulated with lipopolysaccharides. CAVAO also suppressed the phosphorylation of c-Jun N-terminal kinase (JNK) and p38, indicating that mitogen-activated protein kinase (MAPK) signaling pathways were also blocked. The major constituents of CAVAO were characterized as linalool (64.6 ± 0.04%), α-terpineol (7.61 ± 0.03%), (R)-limonene (6.15 ± 0.04%), and linalyl acetate (5.02 ± 0.03%), which might be responsible for its observed anti-inflammation activity. It is concluded that CAVAO has great potential to be developed into a functional food for the treatment of inflammatory-associated diseases.
Keyphrases
- essential oil
- oxidative stress
- signaling pathway
- induced apoptosis
- nuclear factor
- protein kinase
- gene expression
- pi k akt
- nitric oxide
- toll like receptor
- rheumatoid arthritis
- tyrosine kinase
- poor prognosis
- hydrogen peroxide
- dna methylation
- binding protein
- immune response
- human health
- endoplasmic reticulum stress
- combination therapy
- small molecule
- genome wide
- cell death
- inflammatory response
- protein protein
- transcription factor
- replacement therapy