Background

Alpha-Tocopherol (α-TCP), one major form of vitamin E, has been known as a treatment for airway allergic inflammation. However, the role and mechanism of α-TCP in treating allergic rhinitis remains unclear.

Objective

In this study we examined the inhibitory function of α-TCP in a mouse model of allergic rhinitis.

Methods

Allergic phenotype was examined by hematoxylin and eosin staining. Total IgE, OVA-specific IgE, OVA-specific IgG1 and OVA-specific IgG2a levels were examined by ELISA. mRNA expression was measured by qPCR, protein levels were examined by Western Blot.

Results

Histological analysis of the nasal membranes revealed that there was a significant reduction in inflammatory cells appearance in cross-sections in alpha-TCP treatment of Ovalbumin (OVA)-sensitized mice compared to OVA sensitized animals. In addition, eosinophils were significantly reduced in nasal mucosa of alpha-TCP treatment of OVA-sensitized mice compared to the OVA group. Lower total IgE, OVA-specific IgE, OVA-specific IgG1 and OVA-specific IgG2a levels were found in alpha-TCP treatment of OVA-sensitized mice compared to the OVA group. Furthermore, we found that the subepithelial distribution of tryptase positive mast cells was reduced in the alpha-TCP treatment of OVA-sensitized mice. More importantly, the PI3K-PKB pathway was suppressed by α-TCP in mast cells.

Conclusions

Our results demonstrated that α-TCP-mediated suppression of PI3K-PKB activity in mast cells is a potential mechanism of anti-allergic function of α-TCP.

中文翻译：

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在过敏性鼻炎小鼠模型中，α-生育酚的抗过敏功能是通过抑制肥大细胞中的PI3K-PKB活性介导的。

背景

维生素E的一种主要形式是α-生育酚（α-TCP），被认为是一种治疗气道过敏性炎症的方法。然而，α-TCP在治疗变应性鼻炎中的作用和机制尚不清楚。

目的

在这项研究中，我们检查了变应性鼻炎小鼠模型中α-TCP的抑制功能。

方法

通过苏木精和曙红染色检查过敏表型。通过ELISA检查总IgE，OVA特异性IgE，OVA特异性IgG1和OVA特异性IgG2a水平。通过qPCR测量mRNA表达，通过蛋白质印迹检查蛋白质水平。

结果

鼻膜的组织学分析显示，与OVA致敏的动物相比，α-TCP治疗卵清蛋白（OVA）致敏的小鼠的横截面中炎症细胞的出现显着减少。另外，与OVA组相比，α-TCP治疗OVA致敏小鼠的鼻粘膜中嗜酸性粒细胞明显减少。与OVA组相比，在OVA致敏小鼠的α-TCP治疗中发现较低的总IgE，OVA特异性IgE，OVA特异性IgG1和OVA特异性IgG2a水平。此外，我们发现在OVA致敏小鼠的α-TCP治疗中，类胰蛋白酶阳性肥大细胞的上皮下分布减少了。更重要的是，肥大细胞中的α-TCP抑制了PI3K-PKB途径。

结论

我们的结果表明，α-TCP介导的肥大细胞中PI3K-PKB活性的抑制是α-TCP抗过敏功能的潜在机制。