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牛磺酸对过敏性鼻炎的体外和体内抗过敏作用。

In vitro and in vivo Antiallergic Effects of Taurine on Allergic Rhinitis.

机构信息

Department of Otorhinolaryngology, Head and Neck Surgery, Dahua Hospital, Shanghai, China.

Department of Pharmaceutics, School of Pharmacy, Fudan University, Shanghai, China.

出版信息

Int Arch Allergy Immunol. 2020;181(6):404-416. doi: 10.1159/000505209. Epub 2020 May 15.

Abstract

BACKGROUND

The current treatment for allergic rhinitis (AR) is inadequate.

OBJECTIVE

The present study aimed to investigate the therapeutic effect of taurine on AR and to identify the underlying molecular mechanisms.

METHODS

The serum level of the antioxidant enzyme extracellular superoxide dismutase (SOD3) was determined in AR patients and in healthy controls. The antiallergic inflammatory effects of taurine were evaluated in a dinitrophenyl-human serum albumin (DNP-HSA)-stimulated human mast cell line (HMC-1) and in an ovalbumin (OVA)-induced AR mouse model.

RESULTS

Clinically, a reduction in serum level of SOD3 was observed in AR patients. Taurine treatment led to dose-dependent increases in SOD3 at both protein and mRNA levels in HMC-1 cells. SOD3 production was regulated by peroxisome proliferator-activated receptor-γ (PPAR-γ) in response to taurine. SOD3 overexpression inhibited the release of proinflammatory cytokines including tumor necrosis factor-α (, interleukin (IL)-4, and IL-6. Its overexpression also ameliorated the loss of interferon-γ. SOD3 and PPAR-γ influenced inflammatory cytokine production via regulation of the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). An OVA-induced AR animal model study showed that taurine was efficacious in alleviating allergic inflammatory reactions by relieving behavior symptoms of AR mice and reducing eosinophilic and mast cell infiltration into the nasal cavity. In addition, taurine treatment increased the production of SOD3 and PPAR-γ, which, in turn, suppressed expression of proinflammatory cytokines through phosphorylation of ERK1/2.

CONCLUSION

Taurine could potentially serve as a therapeutic treatment for allergic disorders.

摘要

背景

目前过敏性鼻炎(AR)的治疗效果不理想。

目的

本研究旨在探讨牛磺酸治疗 AR 的疗效及其潜在的分子机制。

方法

检测 AR 患者和健康对照者血清抗氧化酶细胞外超氧化物歧化酶(SOD3)水平。在二硝基苯人血清白蛋白(DNP-HSA)刺激的人肥大细胞系(HMC-1)和卵清蛋白(OVA)诱导的 AR 小鼠模型中评估牛磺酸的抗过敏炎症作用。

结果

临床上,AR 患者血清 SOD3 水平降低。牛磺酸治疗可使 HMC-1 细胞中 SOD3 的蛋白和 mRNA 水平呈剂量依赖性增加。SOD3 的产生受过氧化物酶体增殖物激活受体-γ(PPAR-γ)调节,对牛磺酸作出反应。SOD3 的过表达抑制了包括肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-4 和 IL-6 在内的促炎细胞因子的释放。其过表达也改善了干扰素-γ的丧失。SOD3 和 PPAR-γ 通过调节细胞外信号调节激酶 1/2(ERK1/2)的磷酸化来影响炎性细胞因子的产生。OVA 诱导的 AR 动物模型研究表明,牛磺酸通过缓解 AR 小鼠的行为症状和减少嗜酸性粒细胞和肥大细胞浸润鼻腔,有效缓解过敏炎症反应。此外,牛磺酸治疗增加了 SOD3 和 PPAR-γ的产生,从而通过 ERK1/2 的磷酸化抑制促炎细胞因子的表达。

结论

牛磺酸可能是治疗过敏疾病的一种潜在治疗方法。

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