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Journal of Ethnopharmacology 2013-Sep

Effects of magnolialide isolated from the leaves of Laurus nobilis L. (Lauraceae) on immunoglobulin E-mediated type I hypersensitivity in vitro.

Straipsnius versti gali tik registruoti vartotojai
Prisijungti Registracija
Nuoroda įrašoma į mainų sritį
Taehun Lee
Sooryun Lee
Kyeong Ho Kim
Ki-Bong Oh
Jongheon Shin
Woongchon Mar

Raktažodžiai

Santrauka

BACKGROUND

Laurus nobilis L. (Lauraceae) has been used for folk medicines in the Mediterranean area and Europe to treat various disorders including skin inflammation (dermatitis) and asthma.

OBJECTIVE

Our aim was to investigate the scientific evaluation of the compounds from Laurus nobilis L. on immuniglobulin E (IgE)-mediated type I hypersensitivity responses in vitro such as atopic dermatitis and asthma.

METHODS

Seven compounds were isolated and examined for the mast cell stabilizing effect on IgE-sensitized RBL-2H3 mast cells by measuring the β-hexosaminidase activity. In addition, the effects on interleukin (IL)-4 production and IL-5-dependent Y16 early B cell proliferation were investigated as well as their cytotoxic effects on RBL-2H3 cells.

RESULTS

Among the seven isolated compounds, magnolialide attenuated the release of β-hexosaminidase from RBL-2H3 cells with an IC50 value of 20.2 μM, while the other compounds revealed no significant effects at concentrations tested. Furthermore, magnolialide significantly inhibited the IL-4 release with an IC50 value of 18.1 μM and IL-4 mRNA expression with an IC50 value of 15.7 μM in IgE-sensitized RBL-2H3 cells. In addition, the inhibition of IL-5-dependent proliferation of early B cells (Y16 cells) by magnolialide was demonstrated with an IC50 value of 18.4 μM.

CONCLUSIONS

These results suggest that the magnolialide might be a candidate for the treatment of IgE-mediated hypersensitivity responses such as atopic dermatitis and asthma by inhibiting mast cell degranulation, the IL-4 production, and IL-5-dependent early B cell proliferation, key factors in the development and amplification of type I hypersensitivity reactions.

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