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A Novel Anti-Inflammatory Role for Ginkgolide B in Asthma via Inhibition of the ERK/MAPK Signaling Pathway

机译:银杏内酯B通过抑制ERK / MAPK信号通路在哮喘中的新型抗炎作用

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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.
机译:银杏内酯B是银杏叶的抗炎提取物,已用于治疗。它是已知的血小板活化因子(PAF)抑制剂,在哮喘的发病机理中很重要。在这里,哮喘的非感染性小鼠模型用于评估银杏内酯B(GKB)的抗炎能力,并表征GKB与促分裂原活化蛋白激酶(MAPK)途径的相互作用。对卵清蛋白(OVA)致敏并攻击的BALB / c小鼠在接受OVA攻击前一小时接受GKB(40 mg / kg)处理。我们的研究表明,GKB可有效抑制支气管肺泡灌洗液(BALF)中T-helper 2细胞因子的增加,例如白介素(IL)-5和IL-13。此外,与OVA激发组相比,GKB治疗后BALF中的嗜酸性粒细胞计数显着降低。组织学研究表明,GKB实质上抑制了OVA诱导的肺组织嗜酸性粒细胞增多和气道中杯状细胞的粘液过度分泌。这些结果表明银杏内酯B可能用于治疗哮喘,其功效与抑制细胞外调节激酶/ MAPK途径有关。

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    《Molecules》 |2011年第9期|共15页
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