An ovalbumin (OVA)-induced allergic rhinitis (AR) mouse model was established to investigate whether α-Lipoic acid (LA) has a protective effect against upper respiratory tract inflammation. BALB/c mice were sensitized by intraperitoneal injection and challenged by intranasal application of OVA. Mice were orally administered various doses of LA once daily (2, 10, 50 mg/kg) and dexamethasone (Dex; 2.5 mg/kg) 1 h before OVA challenge. Allergic nasal symptoms, levels of OVA-specific immunoglobulins, cytokines, and transcription factors were measured. Nasal and lung histopathology were evaluated. LA administration significantly alleviated the nasal symptoms such as rubbing and sneezing, markedly reduced both serum OVA-specific IgE and IgG1 levels. The LA treatment group showed markedly up-regulated levels of the Treg cytokine IL-10 and Treg transcription factor Foxp3. In contrast, it showed down-regulated levels of the Th17 cytokine IL-17 and the Th17 transcription factor STAT3, and RORγ. LA greatly enhanced the nuclear factor erythroid-derived 2/heme oxygenase 1 (Nrf2/HO-1) pathway signaling and inhibited the activation of NF-κB/IκB, markedly suppressed the levels of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, IL-8 and chemokine COX-2. The histologic alterations of nasal and lung tissues of AR mice were effectively ameliorated by LA. Based on these results, we suggest that LA could be a potential therapeutic agent in OVA-induced AR by virtue of its role in controlling the Th17/Treg balance and enhancing Nrf2/HO-1 pathway signaling.

译文

:建立了卵白蛋白(OVA)诱导的变应性鼻炎(AR)小鼠模型,以研究α-硫辛酸(LA)是否对上呼吸道炎症具有保护作用。通过腹腔注射致敏BALB / c小鼠,并通过鼻内施用OVA攻击。每天向小鼠口服一次不同剂量的LA(2、10、50 mg / kg)和地塞米松(Dex; 2.5 mg / kg)于OVA攻击前1小时。测量过敏性鼻症状,OVA特异性免疫球蛋白,细胞因子和转录因子的水平。评估鼻和肺的组织病理学。 LA给药可显着缓解鼻部症状,如揉搓和打喷嚏,可显着降低血清OVA特异性IgE和IgG1水平。 LA治疗组显示Treg细胞因子IL-10和Treg转录因子Foxp3的水平明显上调。相反,它显示Th17细胞因子IL-17和Th17转录因子STAT3和RORγ的水平下调。 LA大大增强了核因子类红细胞衍生的2 /血红素加氧酶1(Nrf2 / HO-1)信号通路并抑制了NF-κB/IκB的激活,显着抑制了促炎性细胞因子TNF-α,IL-1β的水平,IL-6,IL-8和趋化因子COX-2。 LA有效改善了AR小鼠鼻和肺组织的组织学改变。基于这些结果,我们认为LA可能由于其在控制Th17 / Treg平衡和增强Nrf2 / HO-1信号通路中的作用而可能是OVA诱导的AR的潜在治疗剂。

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