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Cryptotanshinone attenuates allergic airway inflammation through negative regulation of NF-kappa B and p38 MAPK

机译:Cryptotanshinone通过NF-Kappa B和P38 Mapk的负调节衰减过敏气道炎症

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摘要

This study is to determine the role and mechanism of cryptotanshinone (CTS) in allergic airway inflammation. Asthma induced by OVA was established in BALB/c mice. We found increased airway hyperresponsiveness (AHR), increased inflammatory cell infiltration, elevated levels of TNF-alpha, interleukin-1 beta (IL-1 beta), IL-4, IL-5, IL-6 and IL-13, decreased interferon gamma (IFN-gamma) in lung tissue, increased content of total immunoglobulin E (IgE), OVA specific IgE, Eotaxin, ICAM-1, VCAM-1, nuclear factor-kappaB (NF-kappa B) and phosphorylation of p38 MAPK in lung tissue. However, the administration of CTS significantly decreased AHR in asthmatic mice, reduced inflammation around the bronchioles and inflammatory cells around airway, regulated cytokine production, reduced the total IgE and OVA-specific IgE levels, and inhibited NF-kappa B activation and p38 MAPK phosphorylation. In vitro experiments in 16 HBE cells revealed that CTS attenuated CAM-1 and IL-6 expression. These results indicate that CTS alleviates allergic airway inflammation by modulating p38 MAPK phosphorylation and NF-kappa B activation.
机译:该研究是确定Cryptotanshinone(CTS)在过敏气道炎症中的作用和机制。在Balb / C小鼠中建立了OVA诱导的哮喘。我们发现气道高反应性(AHR)增加,炎症细胞浸润,TNF-α的升高,白细胞介素-1β(IL-1β),IL-4,IL-5,IL-6和IL-13降低,减少了干扰素γ(IFN-Gamma)在肺组织中,总免疫球蛋白E(IgE)的含量增加,OVA特异性IgE,ETAXIN,ICAM-1,VCAM-1,核因子-Kappab(NF-Kappa B)和P38 MAPK的磷酸化肺组织。然而,CTS的施用显着降低了哮喘小鼠的AHR,减少了支气管周围的炎症和炎气道的炎症细胞,调节的细胞因子产生,降低总IgE和卵子特异性IgE水平,并抑制NF-Kappa活化和P38 Mapk磷酸化。在16 HBE细胞中的体外实验表明CTS减弱了CAM-1和IL-6表达。这些结果表明,CT通过调节P38 MAPK磷酸化和NF-Kappa B激活来减轻过敏气道炎症。

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