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-α, interleukin-1β (IL-1β), IL-4, IL-5, IL-6 and IL-13, decreased interferon gamma (IFN-γ) in lung tissue, increased content of total immunoglobulin E (IgE), OVA specific IgE, Eotaxin, ICAM-1, VCAM-1, nuclear factor-kappaB (NF-κB) 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-κB 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-κB activation.

中文翻译：

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隐丹参酮通过负调节NF-κB和p38 MAPK减轻过敏性气道炎症。

这项研究旨在确定隐丹参酮（CTS）在过敏性气道炎症中的作用和机制。在BALB / c小鼠中建立了由OVA诱导的哮喘。我们发现气道高反应性（AHR）增加，炎性细胞浸润增加，TNF-α，白介素-1β（IL-1β），IL-4，IL-5，IL-6和IL-13的水平升高，干扰素γ降低（肺组织中的IFN-γ），总免疫球蛋白E（IgE），OVA特异性IgE，Eotaxin，ICAM-1，VCAM-1，核因子-κB（NF-κB）和肺组织中p38 MAPK磷酸化的含量增加。但是，CTS的给药可显着降低哮喘小鼠的AHR，减少细支气管周围的炎症和气道周围的炎症细胞，调节细胞因子的产生，降低总IgE和OVA特异性IgE的水平，并抑制NF-κB活化和p38 MAPK磷酸化。在16个HBE细胞中进行的体外实验表明CTS减弱了CAM-1和IL-6的表达。这些结果表明，CTS通过调节p38 MAPK磷酸化和NF-κB活化减轻了过敏性气道炎症。