TY - JOUR
T1 - Effect of Lavender essential oil on LPS-stimulated inflammation
AU - Huang, Mei Yu
AU - Liao, May Hua
AU - Wang, Yang Kao
AU - Huang, Yung Sheng
AU - Wen, Hsiao Chuan
N1 - Funding Information:
We thank Taiwan Cosmetic Practice Development Association for the financial support and grants from the National Science Council of the Republic of China (grant NSC 96 2622-M-264-003-CC3).
PY - 2012
Y1 - 2012
N2 - Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromatherapy. Many studies have demonstrated its functions in calming, assisting sleep, reducing pain and muscular spasms and its antiseptic function. To date, however, the mechanism of LEO on inflammation response is not well understood. In this study, we examined the effect of LEO on 5 μg/ml lipopolysaccharide (LPS) induced inflammation reaction in human monocyte THP-1 cells. We found treatment of 0.1% LEO significantly increased cell viability and inhibited the IL-1β and superoxide anion generation in LPS-stimulated THP-1 cells. Treatment with LEO down-regulated both LPS-induced protein levels of phospho-NF-κB and membrane Toll-llike receptor 4. To determine whether the chaperone protein was involved in the reaction, we determined the levels of Heat Shock Protein 70 (HSP70). Our results showed that LEO increased HSP70 expression in LPS-stimulated THP-1 cells, suggesting that the LEO inhibited LPS-induced inflammatory effect might be associated with the expression of HSP70.
AB - Lavender essential oil (LEO) is one the most favorite and widely used essential oils in aromatherapy. Many studies have demonstrated its functions in calming, assisting sleep, reducing pain and muscular spasms and its antiseptic function. To date, however, the mechanism of LEO on inflammation response is not well understood. In this study, we examined the effect of LEO on 5 μg/ml lipopolysaccharide (LPS) induced inflammation reaction in human monocyte THP-1 cells. We found treatment of 0.1% LEO significantly increased cell viability and inhibited the IL-1β and superoxide anion generation in LPS-stimulated THP-1 cells. Treatment with LEO down-regulated both LPS-induced protein levels of phospho-NF-κB and membrane Toll-llike receptor 4. To determine whether the chaperone protein was involved in the reaction, we determined the levels of Heat Shock Protein 70 (HSP70). Our results showed that LEO increased HSP70 expression in LPS-stimulated THP-1 cells, suggesting that the LEO inhibited LPS-induced inflammatory effect might be associated with the expression of HSP70.
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U2 - 10.1142/S0192415X12500632
DO - 10.1142/S0192415X12500632
M3 - Article
C2 - 22809036
AN - SCOPUS:84864234119
SN - 0192-415X
VL - 40
SP - 845
EP - 859
JO - American Journal of Chinese Medicine
JF - American Journal of Chinese Medicine
IS - 4
ER -