咽后清配方通过上调卵黄蛋白诱导的哮喘小鼠的Treg抑制Th2反应减轻过敏性气道炎症
2019/03/21
民族药学关联:咽后清(YHQ)配方是包含14种成分的中药,用于咽炎和咳嗽的中药治疗。本研究在卵清蛋白(OVA)诱导的过敏性哮喘小鼠模型中探讨YHQ抑制气道高反应性(AHR)的抗过敏作用及其机制。
方法和试验:BALB/c小鼠经卵清蛋白和霍乱毒素(CT)致敏,经卵清蛋白鼻腔刺激诱导过敏性哮喘小鼠模型。从卵清蛋白致敏的第2周开始口服YHQ(200 毫克/公斤)3周。肺组织的AHR和组织学变化分别采用全身气压胸透分析和苏木精、伊红(H&E)染色。采用酶联免疫吸附法(ELISA)检测OVA特异性IgE和2型辅助性T细胞 (Th2)细胞因子(IL-4和IL-13)的血清浓度。流式细胞术检测脾脏CD4+CD25+Foxp3+调节性T细胞(Treg)的百分比。
结果:过敏性哮喘组AHR反应升高,炎性细胞浸润加重,Th2细胞因子升高,提示成功建立了卵清蛋白诱导哮喘小鼠模型。与过敏性哮喘组相比,OVA诱导的AHR反应和肺内嗜酸性粒细胞浸润明显改善,YHQ治疗后血清中OVA特异性IgE和Th2细胞因子IL-4、IL-13的生成也明显降低。YHQ治疗明显增加OVA诱导的过敏性哮喘小鼠模型中CD4+CD25+Foxp3+ Treg的比例。
结论:YHQ通过促进小鼠模型中CD4+CD25+Foxp3+ Treg的表达,抑制Th2反应,改善过敏性哮喘相关症状,提示YHQ可作为缓解过敏性哮喘相关症状的有效药物。
(J Ethnopharmacol. 2019 Mar 1;231:275-282.)
Yan-Hou-Qing formula attenuates allergic airway inflammation via up-regulation of Treg and suppressing Th2 responses in Ovalbumin-induced asthmatic mice.
Cheng BH, Hu TY, Mo LH, Ma L, Hu WH, Li YS, Liu ZQ, Qiu SQ.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Yan-Hou-Qing (YHQ), a Chinese medicine formula containing fourteen kinds of materials, has been designed for pharyngitis and cough treatment in Oriental medicine. In the present study, the anti-allergic effects and underlying mechanisms of YHQ in inhibition of airway hyper responsiveness (AHR) was explored in an ovalbumin (OVA)-induced allergic asthma mouse model.
MATERIALS AND METHODS: BALB/c mice were sensitized by OVA and cholera toxin (CT) and challenged with OVA intranasally to induce allergic asthma mouse model. YHQ (200 mg/kg) was orally administered for 3 weeks from week-2 after OVA sensitization. The AHR and histological changes of lung tissues were evaluated by whole-body barometric plethysmography analysis and hematoxylin and eosin (H&E) staining, respectively. The serum concentration of OVA-specific IgE and T helper 2 (Th2) cytokines (IL-4 and IL-13) were determined by enzyme-linked immune sorbent assay (ELISA). Flow cytometry was performed to evaluate the percentage of CD4+CD25+Foxp3+ regulatory T cells (Treg) in the spleen.
RESULTS: The elevated AHR responses, heavier inflammatory cell infiltration and Th2 cytokines in allergic asthma group indicated Ovalbumin-induced asthmatic mouse models were built successfully. Compared to allergic asthma group, OVA-induced AHR responses and eosinophil infiltration in lung were improved significantly, and the productions of OVA-specific IgE and Th2 cytokines, IL-4 and IL-13, in the serum were also reduced dramatically after the treatment of YHQ. Moreover, YHQ treatment significantly increased the percentage of CD4+CD25+Foxp3+ Treg in OVA-induced allergic asthma mouse model.
CONCLUSIONS: YHQ improves the allergic asthma related symptoms via promotion of CD4+CD25+Foxp3+ Treg and suppression of Th2 responses in mouse model, suggesting YHQ can be used as a potent agent to alleviate allergic asthma related symptoms.
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