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. 2013 May 22;18(5):6113-27.
doi: 10.3390/molecules18056113.

The ameliorative effect of sophoricoside on mast cell-mediated allergic inflammation in vivo and in vitro

Su-Jin Kim  1 , Gil-Yong Lee, Ji-Wook Jung, Sa-Rang Oh, Eun-Mi Ahn, Sung-Hoon Kim, Seung-Heon Hong, Jae-Young Um
Affiliations

The ameliorative effect of sophoricoside on mast cell-mediated allergic inflammation in vivo and in vitro

Su-Jin Kim et al. Molecules. .

Abstract

Sophoricoside exhibits numerous pharmacological effects, including anti- inflammatory and anti-cancer actions, yet the exact mechanism that accounts for the anti-allergic effects of sophoricoside is not completely understood. The aim of the present study was to elucidate whether and how sophoricoside modulates the mast cell-mediated allergic inflammation in vitro and in vivo. We investigated the pharmacological effects of sophoricoside on both compound 48/80 or histamine-induced scratching behaviors and 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in mice. Additionally, to find a possible explanation for the anti-inflammatory effects of sophoricoside, we evaluated the effects of sophoricoside on the production of histamine and inflammatory cytokines and activation of nuclear factor-κB (NF-κB) and caspase-1 in phorbol 12-myristate 13-acetate plus calcium ionophore A23187 (PMACI)-stimulated human mast cells (HMC-1). The finding of this study demonstrated that sophoricoside reduced compound 48/80 or histamine-induced scratching behaviors and DNCB-induced atopic dermatitis in mice. Additionally, sophoricoside inhibited the production of inflammatory cytokines as well as the activation of NF-κB and caspase-1 in stimulated HMC-1. Collectively, the findings of this study provide us with novel insights into the pharmacological actions of sophoricoside as a potential molecule for use in the treatment of allergic inflammation diseases.

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Figures

Figure 1
Figure 1
Chemical structure of sophoricoside.
Figure 2
Figure 2
Effect of sophoricoside on scratching behavior in ICR mice. (A,B) Sophoricoside (2 mg/kg) was orally administered 1 h before compound 48/80 (50 µg/kg) or histamine (100 µg/kg) intradermally injection. Scratching behaviors was counted as one incident of scratching for 30 min. Terfenadine (10 mg/kg) was used as a positive control. Each datum represents the means ± S.E.M. of three independent experiments (# p < 0.05 vs. control group, * p < 0.05 vs. compound 48/80 or histamine-treated group).
Figure 3
Figure 3
Effect of sophoricoside on the DNCB-induced atopic dermatitis and serum IgE level. (A) The BALB/c mice (n = 6) were sensitized with 100 μL of 0.1% DNCB in acetone/olive oil (3:1) or vehicle [acetone/olive oil (3:1)] applied to the dorsal skin twice each week for a total period of 5 weeks. After 3 weeks, sophoricoside (2 mg/kg) was orally administered 2 week prior to the end of the experiment; (B) Blood samples were collected and then levels of serum IgE in the indicated groups were measured using ELISA method. Each datum represents the means ± S.E.M. of three independent experiments (# p < 0.05 vs. control group, * p < 0.05 vs. DNCB -treated group).
Figure 4
Figure 4
Effect of sophoricoside on histamine release from in PMACI-stimulated HMC-1 cells. Cells (6 × 105 cells/well) were pretreated with various concentrations of sophoricoside (1–50 µM) for 1 h and then treated with PMACI (50 µM PMA + 1 µg/mL A23187) for 4 h. (A) The histamine content was measured by the histamine assay kit as described under material and methods; (B) Cells (3 × 105 cells/well) were pretreated with various concentrations of sophoricoside (1–50 µM) for 1 h and then treated with PMACI for 12 h. Cell viability was evaluated by a MTT colorimetric assay. All data were represented in the mean ± S.E.M. of triplicate determinations from triplicate separate experiments (# p < 0.05 vs. control, * p < 0.05 vs. PMACI alone).
Figure 5
Figure 5
Effects of sophoricoside on the production of inflammatory cytokines in PMACI-stimulated HMC-1 cells. Cells (5 × 105 cells/well) were pre-treated with sophoricoside (1–50 µM) for 1 h and then stimulated PMACI (50 µM PMA + 1 µg/mL A23187) for 12 h. The levels of inflammatory cytokines (TNF-α, IL-8 and IL-6) were measured from cell supernatant using ELISA. All data were represented in the mean ± S.E.M. of triplicate determinations from triplicate separate experiments (# p < 0.05 vs. control, * p < 0.05 vs. PMACI alone).
Figure 6
Figure 6
Effect of sophoricoside on the NF-κB activation in the nuclei of PMACI-stimulated HMC-1 cells. Cells(6 × 106 cells/well) were pre-treated with sophoricoside (50 µM) for 1 h and then stimulated with PMACI (50 µM PMA + 1 µg/mL A23187) for 2 h. Dexamethason (50 µM) was used as a positive control. (A) Nuclear and cytosol extracts were prepared as described in the Materials and Methods section and evaluated for RelA/p65 via Western blot analysis; (B) The relative levels of NF-κB were represented; (C) The cells were fixed, and stained with TRITC-conjugated phalloidin (NF-κB, red) and DAPI (nuclear, blue), and examined under an Olympus microscope (Magnification ×100). All data were represented in the mean ± S.E.M. of triplicate determinations from triplicate separate experiments (# p < 0.05 vs. control, * p < 0.05 vs. PMACI alone).
Figure 7
Figure 7
Effect of sophoricoside on caspase-1 activation in PMACI-stimulated HMC-1. The cells were pretreated with sophoricoside (1–50 µM) for 1 h prior to PMACI stimulation for 4 h. Dexamethasone (50 µM) was used as a positive control. The enzymatic activity of caspase-1 was tested by a caspase-1 colorimetric assay. All data were represented in the mean ± S.E.M. of triplicate determinations from triplicate separate experiments (# p < 0.05 vs. control, * p < 0.05 vs. PMACI alone).
Figure 8
Figure 8
Proposed anti-inflammatory mechanism of sophoricoside in HMC-1.
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