Abstract
Ginkgolide B is an anti-inflammatory extract of Ginkgo biloba and has been used therapeutically. It is a known inhibitor of platelet activating factor (PAF), which is important in the pathogenesis of asthma. Here, a non-infectious mouse model of asthma is used to evaluate the anti-inflammatory capacity of ginkgolide B (GKB) and characterize the interaction of GKB with the mitogen activated protein kinase (MAPK) pathway. BALB/c mice that were sensitized and challenged to ovalbumin (OVA) were treated with GKB (40 mg/kg) one hour before they were challenged with OVA. Our study demonstrated that GKB may effectively inhibit the increase of T-helper 2 cytokines, such as interleukin (IL)-5 and IL-13 in bronchoalveolar lavage fluid (BALF). Furthermore, the eosinophil count in BALF significantly decreased after treatment of GKB when compared with the OVA-challenged group. Histological studies demonstrated that GKB substantially inhibited OVA-induced eosinophilia in lung tissue and mucus hyper-secretion by goblet cells in the airway. These results suggest that ginkgolide B may be useful for the treatment of asthma and its efficacy is related to suppression of extracellular regulating kinase/MAPK pathway.
Highlights
Asthma is a complex disease characterized by acute and chronic airway inflammation, airway hyper-responsiveness (AHR), eosinophilia and mucus hypersecretion by goblet cells
Based on studies investigating the effect of ginkgolide B (GKB), no available study has been done in a mouse model of allergic airway inflammation, so we focused on investigating whether GKB possesses a distinct anti-inflammatory activity on a non-infectious mouse model of asthma, and elucidated the involvement with mitogen activated protein kinase (MAPK) pathway for the first time
Treatment with GKB caused a reduction in the levels of IL-5 and IL-13 compared to ovalbumin-immunized mice (Figure 1)
Summary
Asthma is a complex disease characterized by acute and chronic airway inflammation, airway hyper-responsiveness (AHR), eosinophilia and mucus hypersecretion by goblet cells. Many cytokines contribute to this inflammation mediated by T-helper 2 (Th2) cells, which play central roles in the pathogenesis of allergic asthma [1,2]. Interleukin (IL)-5 expressed by Th2 cells, is responsible for eosinophil growth, differentiation, mobilization, recruitment, activation, and survival [3,4,5]. Interleukin (IL)-13 play an important role in T-cell differentiation toward a Th2 phenotype and isotype switching of B cells to immunoglobulin IgE production [6,7]. Interleukin (IL)-13 promotes acute inflammatory processes and underlying structural changes to the airways [8].
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