首页> 美国卫生研究院文献>other >Perilla frutescens Leaf Extract Inhibits Mite Major Allergen Der p 2-induced Gene Expression of Pro-Allergic and Pro-Inflammatory Cytokines in Human Bronchial Epithelial Cell BEAS-2B
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Perilla frutescens Leaf Extract Inhibits Mite Major Allergen Der p 2-induced Gene Expression of Pro-Allergic and Pro-Inflammatory Cytokines in Human Bronchial Epithelial Cell BEAS-2B

机译:紫苏叶提取物抑制螨主要过敏原Der p 2诱导的人支气管上皮细胞BEAS-2B的过敏原和炎性细胞因子的基因表达

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摘要

Perilla frutescens has been used in traditional medicine for respiratory diseases due to its anti-bacterial and anti-inflammatory activity. This study aimed to investigate effects of Perilla frutescens leaf extract (PFE) on expression of pro-allergic and pro-inflammatory cytokines in airway epithelial cells exposed to mite major allergen Der p 2 (DP2) and the underlying mechanisms. Our results showed that PFE up to 100 µg/mL had no cytotoxic effect on human bronchial epithelial cell BEAS-2B. Further investigations revealed that PFE dose-dependently diminished mRNA expression of pro-allergic cytokine IL-4, IL-5, IL-13 and GM-CSF, as well as pro-inflammatory cytokine IL-6, IL-8 and MCP-1 in BEAS-2B cells treated with DP2. In parallel to mRNA, the DP-2-elevated levels of the tested cytokines were decreased. Further investigation showed that DP2-indued phosphorylation of p38 MAPK (P38) and JNK, but not Erk1/2, was also suppressed by PFE. In addition, PFE elevated cytosolic IκBα level and decreased nuclear NF-κB level in DP2-stimulated BEAS-2B cells. Taken together, these findings revealed that PFE significantly diminished both mRNA expression and protein levels of pro-allergic and pro-inflammatory cytokines in response to DP2 through inhibition of P38/JNK and NK-κB activation. These findings suggest that PFE should be beneficial to alleviate both allergic and inflammatory responses on airway epithelium in response to aeroallergens.
机译:紫苏由于其抗菌和消炎作用,已被用于呼吸系统疾病的传统医学中。这项研究旨在调查紫苏叶提取物(PFE)对暴露于螨主要过敏原Der p 2(DP2)的气道上皮细胞中促过敏和促炎细胞因子表达的影响及其潜在机制。我们的结果表明,高达100 µg / mL的PFE对人支气管上皮细胞BEAS-2B没有细胞毒性作用。进一步的研究表明,PFE剂量依赖性地降低了变应原性细胞因子IL-4,IL-5,IL-13和GM-CSF以及促炎性细胞因子IL-6,IL-8和MCP-1的mRNA表达。 DP2处理过的BEAS-2B细胞中的抗性。与mRNA平行,被测细胞因子的DP-2升高水平降低。进一步的研究表明,PFE还抑制了DP2诱导的p38 MAPK(P38)和JNK的磷酸化,但未抑制Erk1 / 2。此外,PFE在DP2刺激的BEAS-2B细胞中增加了胞浆IκBα水平,并降低了核NF-κB水平。综上所述,这些发现表明,PFE通过抑制P38 / JNK和NK-κB的活化,显着降低了对DP2的过敏和促炎性细胞因子的mRNA表达和蛋白水平。这些发现表明,PFE应该有益于缓解气道上皮对气敏性变应原的过敏和炎症反应。

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