Abstract
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.
Highlights
Abbreviations AR Allergic rhinitis Dex Dexamethasone Foxp[3] Factor forkhead box P3 HO-1 Heme oxygenase-1 Ig Immunoglobulin IL Interleukin lipoic acid (LA) α-Lipoic acid MDA Malondiadehyde NALF Nasal lavage fluid Nrf[2] Nuclear factor-like 2 OVA Ovalbumin RORγ RAR-related orphan receptor gamma
Our study showed that the level of MDA was significantly increased in the OVA group compared with that in the control group, and it was sharply decreased by LA administration (Fig. 8A)
Repeated triggering of the allergic inflammatory response results in the IgE antibody binding to mast cells and basophils, leading to degranulation and release of preformed mediators such as histamine, leukotrienes, and prostaglandin D222
Summary
Abbreviations AR Allergic rhinitis Dex Dexamethasone Foxp[3] Factor forkhead box P3 HO-1 Heme oxygenase-1 Ig Immunoglobulin IL Interleukin LA α-Lipoic acid MDA Malondiadehyde NALF Nasal lavage fluid Nrf[2] Nuclear factor (erythroid-derived 2)-like 2 OVA Ovalbumin RORγ RAR-related orphan receptor gamma. Recent evidence has revealed the roles of Th17 cells and their cytokines in promoting both eosinophilic and neutrophilic increase in the development of allergic disease[6]. Treg cells may be able to inhibit Th2/Th17 responses in allergic diseases[8] Oxidative stress and their production of reactive oxygen species (ROS) were reported to associate with the development of several allergic inflammation diseases included A R9. The antioxidant properties of LA have been linked to several benefits, including lower blood sugar levels, reduced inflammation, slowed skin aging, and improved nerve function[14]. It has been described as a modulator of various inflammatory signaling pathways[15]. We investigated the effect of LA treatment on allergic responses in an OVA-induced AR mouse model
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