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首页> 外文期刊>Clinical and Experimental Otorhinolaryngology >Antiallergic Effects of Trichostatin A in a Murine Model of Allergic Rhinitis
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Antiallergic Effects of Trichostatin A in a Murine Model of Allergic Rhinitis

机译：Trichostatin A在变应性鼻炎小鼠模型中的抗过敏作用

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Objectives Trichostatin A (TSA), an inhibitor of histone deacetylase, has been shown to play an important role in attenuating asthmatic inflammation. However, the effect of TSA in allergic rhinitis is not known. The aims of this study were to investigate the effect of TSA on allergic nasal inflammation and on the induction of regulatory T cells in a murine model of allergic rhinitis. Methods BALB/c mice were sensitized intraperitoneally with ovalbumin (OVA) and then challenged intranasally with OVA. TSA (1 mg/kg) was given to the treatment group, and multiple parameters of allergic responses were evaluated to determine the effects of TSA on allergic rhinitis. Allergic nasal symptom scores, including frequency of rubbing and sneezing, were checked. Eosinophil infiltrations were stained with Chromotrope 2R, and the expression levels of OVA-specific IgE, T-helper 1 (Th1) cytokine (interferon-gamma [IFN-γ]), Th2 cytokines (interleukin [IL] 4 and IL-5) and Treg (Foxp3, IL-10, and transforming growth factor-beta [TGF-β]) were measured by quantitative reverse transcription-polymerase chain reaction or enzyme-linked immunosorbent assay. Results TSA reduced the scores of allergic nasal symptoms and the amount of eosinophil infiltration into the nasal mucosa. TSA suppressed OVA-specific IgE levels and reduced expression of the IL-4 and IL-5. However, the expression of IFN-γ was unchanged in the treatment group. The levels of Foxp3, IL-10, and TGF-β were increased in pretreatment with TSA as compared to control group. Conclusion This study shows that TSA induced antiallergic effects by decreasing eosinophilic infiltration and Th2 cytokines in a murine model of allergic rhinitis via regulation of Tregs. Thus, TSA may be considered a potentially therapeutic agent in treating allergic rhinitis.
机译：目的已证明组蛋白脱乙酰基酶抑制剂曲古他汀A（TSA）在减轻哮喘炎症中起重要作用。然而，TSA在变应性鼻炎中的作用尚不清楚。这项研究的目的是调查在过敏性鼻炎的小鼠模型中TSA对过敏性鼻炎症的影响以及对调节性T细胞的诱导作用。方法用卵清蛋白（OVA）腹膜内敏化BALB / c小鼠，然后用OVA鼻内攻击。将TSA（1 mg / kg）给予治疗组，并评估过敏反应的多个参数，以确定TSA对过敏性鼻炎的影响。检查过敏性鼻症状评分，包括揉搓和打喷嚏的频率。嗜酸性粒细胞浸润用Chromotrope 2R染色，OVA特异性IgE，T辅助1（Th1）细胞因子（干扰素-γ[IFN-γ]），Th2细胞因子（白介素[IL] 4和IL-5）的表达水平通过定量逆转录-聚合酶链反应或酶联免疫吸附测定法测定Treg（Foxp3，IL-10和转化生长因子-β[TGF-β]）。结果TSA减少了过敏性鼻症状的得分和嗜酸性粒细胞浸入鼻粘膜的数量。 TSA抑制了OVA特异性IgE水平，并降低了IL-4和IL-5的表达。但是，在治疗组中IFN-γ的表达没有变化。与对照组相比，TSA预处理组Foxp3，IL-10和TGF-β的水平升高。结论：本研究表明，TSA通过调节Tregs降低了变应性鼻炎小鼠模型中的嗜酸性细胞浸润和Th2细胞因子，从而诱导了抗过敏作用。因此，TSA可以被认为是治疗变应性鼻炎的潜在治疗剂。

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