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首页> 外文期刊>International immunopharmacology >Therapeutic effects of R8, a semi-synthetic analogue of Vasicine, on murine model of allergic airway inflammation via STAT6 inhibition
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Therapeutic effects of R8, a semi-synthetic analogue of Vasicine, on murine model of allergic airway inflammation via STAT6 inhibition

机译：R8是Vasicine的半合成类似物，通过STAT6抑制作用对变应性气道炎症的鼠模型产生治疗作用

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This is a follow-up study of our previous work in which we screened a series of Vasicine analogues for their anti-inflammatory activity in a preventive OVA induced murine model of asthma. The study demonstrated that R8, one of the analogues, significantly suppressed the Th2 cytokine production and eosinophil recruitment to the airways. In the present study, we have been using two standard experimental murine models of asthma, where the mice were treated with R8 either during (preventive use) or after (therapeutic use) the development of asthma features. In the preventive model, R8 reduced inflammatory cell infiltration to the airways, OVA specific IgE and Th2 cytokine production. Also, the R8 treatment in the therapeutic model decreased methacholine induced AHR, Th2 cytokine release, serum IgE levels, infiltration of inflammatory cells into the airways, phosphorylation of STAT6 and. expression of GATA3. Moreover, R8 not only reduced goblet cell metaplasia in asthmatic mice but also reduced IL-4 induced Muc5AC gene expression in human alveolar basal epithelial cells. Further, R8 attenuated IL-4 induced differentiation of murine splenocytes into Th2 cells in vitro. So, we may deduce that R8 treatment profoundly reduced asthma features by attenuating the differentiation of T cells into Th2 cells by interfering with the binding of IL-4 to its receptor in turn decreasing the phosphorylation of STAT6 and expression of GATA3 in murine model of asthma. These preclinical findings suggest a possible therapeutic role of R8 in allergic asthma. (c) 2015 Elsevier B.V. All rights reserved.
机译：这是对我们先前工作的后续研究，其中我们在预防性OVA诱发的小鼠哮喘模型中筛选了一系列Vasicine类似物的抗炎活性。研究表明，R8是类似物之一，可显着抑制Th2细胞因子的产生和嗜酸性粒细胞向呼吸道的募集。在本研究中，我们一直在使用两个标准的哮喘实验鼠模型，其中在哮喘特征发作期间（预防性使用）或之后（治疗性使用）用R8治疗小鼠。在预防模型中，R8减少了炎症细胞向气道的浸润，OVA特异性IgE和Th2细胞因子的产生。而且，在治疗模型中的R8治疗降低了甲胆碱诱导的AHR，Th2细胞因子释放，血清IgE水平，炎性细胞向气道的浸润，STAT6的磷酸化等。 GATA3的表达。而且，R8不仅减少了哮喘小鼠的杯状细胞化生，而且减少了IL-4诱导的人肺泡基底上皮细胞中Muc5AC基因的表达。此外，R8减弱了IL-4诱导的小鼠脾细胞在体外向Th2细胞的分化。因此，我们可以推断出R8治疗可通过干扰IL-4与其受体的结合而减弱T细胞向Th2细胞的分化，进而降低哮喘小鼠模型中STAT6的磷酸化和GATA3的表达，从而显着降低哮喘的特征。 。这些临床前发现表明，R8在过敏性哮喘中可能具有治疗作用。 （c）2015 Elsevier B.V.保留所有权利。

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