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Sesamin attenuates allergic airway inflammation through the suppression of nuclear factor-kappa B activation

机译:芝麻素通过抑制核因子-κB活化来减轻过敏性气道炎症

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摘要

The aim of the present study is to determine the role of sesamin, the most abundant lignan in sesame seed oil, on the regulation of allergic airway inflammation in a murine asthma model. A BALB/c mouse model with allergic asthma was used to evaluate the effects of sesamin on nuclear factor-kappa B (NF-κB) activation. An enzyme-linked immunosorbent assay was used to determine protein expression in bronchoalveolar lavage (BAL) fluids. Hematoxylin and eosin staining was performed to examine histological changes. Moreover, western blot analysis was used to detect the expression of proteins in tissues. Prior to administering sesamin, the mice developed the following pathophysiological features of asthma: An increase in the number of inflammatory cells, increased levels of interleukin (IL)-4, IL-5 and IL-13, decreased levels of interferon-γ in BAL fluids and lung tissues, increased immunoglobulin E (IgE) levels in the serum and an increased activation of NF-κB in lung tissues. Following treatment with sesamin, the mice had evidently reduced peribronchiolar inflammation and airway inflammatory cell recruitment, inhibited production of several cytokines in BAL fluids and lung tissues, and decreased IgE levels. Following inhalation of ovalbumin, the administration of sesamin also inhibited the activation of NF-κB. In addition, sesamin administration reduced the phosphorylation of p38 mitogen-activated protein kinases (MAPKs). The present study demonstrates that sesamin decreases the activation of NF-κB in order to attenuate allergic airway inflammation in a murine model of asthma, possibly via the regulation of phosphorylation of p38 MAPK. These observations provide an important molecular mechanism for the potential use of sesamin in preventing and/or treating asthma, as well as other airway inflammatory disorders.
机译:本研究的目的是确定芝麻籽油中最丰富的木脂素芝麻素对鼠哮喘模型中过敏性气道炎症的调节作用。使用BALB / c过敏性哮喘小鼠模型评估芝麻素对核因子-κB(NF-κB)活化的影响。酶联免疫吸附试验用于确定支气管肺泡灌洗液(BAL)中的蛋白质表达。进行苏木精和曙红染色以检查组织学变化。此外,蛋白质印迹分析用于检测组织中蛋白质的表达。在使用芝麻素之前,小鼠出现以下哮喘的病理生理特征:炎症细胞数量增加,白细胞介素(IL)-4,IL-5和IL-13水平升高,BAL中干扰素-γ水平降低体液和肺组织中,血清中免疫球蛋白E(IgE)水平升高,肺组织中NF-κB活化增加。用芝麻素处理后,小鼠明显减少了支气管周围炎症和气道炎症细胞募集,抑制了BAL液和肺组织中几种细胞因子的产生,并降低了IgE水平。吸入卵清蛋白后,芝麻素的给药也抑制了NF-κB的活化。此外,芝麻素的给药减少了p38丝裂原活化蛋白激酶(MAPKs)的磷酸化。本研究表明,芝麻素可能通过调节p38 MAPK的磷酸化来降低哮喘小鼠模型中的过敏性气道炎症,从而降低NF-κB的活化。这些观察结果为芝麻素在预防和/或治疗哮喘以及其他气道炎性疾病中的潜在用途提供了重要的分子机制。

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