4.7 Article

Effects of lactose-β-sitosterol and β-sitosterol on ovalbumin-induced lung inflammation in actively sensitized mice

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 7, Issue 12, Pages 1517-1527

Publisher

ELSEVIER
DOI: 10.1016/j.intimp.2007.07.026

Keywords

lactose-beta-sitosterol; beta-sitosterol; asthma

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Asthma is a disease marked by chronic lung inflammation and the number of patients suffering from asthma increases annually. Both -sitosterol BS, and I-sitosterol glucoside exist it, a variety of plants and have anti-tumor, anti-microbial, and immunomodulatory activities. However, the precise role of BS and -sitosterol glucoside in asthma has not been well understood. The aim of this study was to investigate the inhibitory effects of BS and lactose-BS (L-BS) on the pathophysiological process in ovalbumin-induced asthmatic mice. The total cells and eosinophils in the bronchoalveolar lavage (BAL) fluid markedly decreased (p<0.05) after L-BS or BS administration (1 mg/kg; i.p.), and the ROS production also decreased in comparison to the asthma control. Histopathological features were detected by performing histochemisty, including H&E and alcian blue & P.A.S staining. Both L-BS and BS mitigated the inflammation by eosinophil infiltration and mucus hypersecretion by goblet hyperplasia. These effects of L-BS were superior to those of BS. L-BS and BS inhibited the increased mRNA and protein expression of IL-4 and IL-5 in the lung tissue and BAL fluid, respectively. The IgE concentration in the BAL fluid and serum was measured by performing ELISA and the ovalbumin-specific IgE in the BAL fluid was uniquely inhibited by L-BS (p<0.05). The splenocytes were isolated from the normal and asthmatic mice and incubated in the absence and presence of 100 mu g/ml ovalbumin, respectively. L-BS blocked the survival rate of the splenocytes of the mice (p<0.01). This finding indicates the possibility of L-BS and BS as potential therapeutic molecules in asthma and may contribute to the need to improve current therapeutic drugs. (C) 2007 Published by Elsevier B.V.

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