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多糖通过抑制 NLRP3 炎性小体激活和 NOD2 介导的 NF-B 激活减轻卵清蛋白诱导的大鼠变应性鼻炎。

Polysaccharides Attenuate Ovalbumin-Induced Allergic Rhinitis in Rats by Inhibiting NLRP3 Inflammasome Activation and NOD2-Mediated NF-B Activation.

机构信息

The First Clinical Medical College; Guangzhou, China.

Department of Pharmacy, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.

出版信息

J Med Food. 2021 Jan;24(1):1-9. doi: 10.1089/jmf.2020.4750. Epub 2020 Dec 23.

DOI:10.1089/jmf.2020.4750
PMID:33370169
Abstract

Allergic rhinitis (AR) is an IgE-mediated chronic inflammatory disease of the allergic nasal mucosa. It has a significant effect on quality life; most patients with AR also suffer from sleep disorders, mood disorders, and deterioration in social relationships. As increasing numbers of medicinal plants show productive anti-inflammatory activity against inflammatory diseases, there is growing interest in natural medicinal plant ingredients. To this end, we selected polysaccharides (APS) to evaluate its anti-inflammatory effect on ovalbumin-induced AR rats, and we further explored its impact on NLRP3 inflammasome activation and NOD2-mediated NF-B activation. We found that APS can alleviate the nasal symptom of AR rats and attenuate pathological alterations. APS also reduced the inflammatory cytokine levels. APS not only inhibited the NLRP3 inflammasome activation but also inhibited NF-B activation by decreasing NOD2 expression and blocking the phosphorylation of NF-B (p65). In conclusion, APS can effectively improve the inflammatory symptoms of nasal mucosa in AR rats, which may be mediated by the inhibition of NLRP3 inflammasome activation and NOD2-mediated NF-B activation. These findings indicate that APS has the potential to be used as a therapeutic agent for AR.

摘要

变应性鼻炎(AR)是一种 IgE 介导的过敏鼻黏膜慢性炎症性疾病。它对生活质量有重大影响;大多数 AR 患者还患有睡眠障碍、情绪障碍和社交关系恶化。由于越来越多的药用植物显示出对炎症性疾病的有效抗炎活性,因此人们对天然药用植物成分的兴趣日益浓厚。为此,我们选择了多糖(APS)来评估其对卵清蛋白诱导的 AR 大鼠的抗炎作用,并进一步探讨其对 NLRP3 炎性小体激活和 NOD2 介导的 NF-B 激活的影响。我们发现 APS 可以缓解 AR 大鼠的鼻部症状并减轻病理改变。APS 还降低了炎症细胞因子水平。APS 不仅抑制了 NLRP3 炎性小体的激活,而且通过降低 NOD2 表达和阻断 NF-B(p65)的磷酸化来抑制 NF-B 激活。总之,APS 可以有效改善 AR 大鼠鼻黏膜的炎症症状,这可能是通过抑制 NLRP3 炎性小体激活和 NOD2 介导的 NF-B 激活来介导的。这些发现表明 APS 有可能被用作 AR 的治疗剂。

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