益气固本方通过TLR4/NF-κB信号通路减轻OVA诱导的哮喘小鼠的气道炎症和气道重塑。

IF 2.8 4区 医学 Q2 PHARMACOLOGY & PHARMACY
Yibu Kong, Zhongtian Wang, Hongjun Yu, Aiai Dong, Yongfu Song, Lei Guo, Jinpu Zhu, Liping Sun, Yinan Guo
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引用次数: 0

摘要

背景:目的:研究益气固本方(YQGB)对卵清蛋白(OVA)诱导的哮喘模型气道炎症和气道重塑的影响,进一步探讨YQGB治疗过敏性哮喘的潜在机制:小鼠随机分为五组(n = 10):对照组、OVA组、OVA + Dex(0.1 mg/kg)组、OVA + 低剂量(1.1 g/kg)YQGB组和OVA + 高剂量(2.2 g/kg)YQGB组。支气管肺泡灌洗液(BALF)中检测到炎性细胞计数和 IgE。通过 H&E、PAS、Masson 和免疫组化染色观察肺组织病理学,并应用 qRT-PCR 和 Western 印迹分析与 TLR4 和 NF-κB 信号通路相关的关键基因和蛋白:结果:在 OVA 诱导的哮喘小鼠中,YQGB 降低了 BALF 中的嗜酸性粒细胞和 IgE。YQGB 缓解了 OVA 诱导的炎症浸润,并降低了 IL-4、IL-5、IL-13、Eotaxin、ECP、GM-CSF、LTC4 和 LTD4。YQGB 可减轻 OVA 诱导的上睑腺细胞增生和粘液分泌过多。YQGB 可减轻 OVA 诱导的上皮下纤维化,并降低 TGF-β1、E-Cadherin、Vimentin 和 Fibronectin。YQGB 可改善 OVA 诱导的气道平滑肌增厚,降低 α-SMA 和 PDGF 水平。YQGB 降低了 TLR4、MyD88、TRAF6、IκBα 和 p65 mRNA 的表达,IκBα 和 p-p65 蛋白水平也有所降低:结论:YQGB通过抑制TLR4/NF-κB信号通路,减轻气道炎症和气道重塑,具有抗哮喘作用,值得临床推广。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
YiQi GuBen formula alleviates airway inflammation and airway remodeling in OVA-induced asthma mice through TLR4/NF-κB signaling pathway.

Background: We aim to investigate the effect of YiQi GuBen formula (YQGB) on airway inflammation and airway remodeling in the ovalbumin (OVA)-induced asthma model to further explore the potential mechanisms of YQGB in treating allergic asthma.

Methods: Mice were divided into five groups randomly (n = 10): the control group, OVA group, OVA + Dex (0.1 mg/kg) group, OVA + low-dose (1.1 g/kg) YQGB group, and OVA + high-dose (2.2 g/kg) YQGB group. Inflammatory cell count and IgE were detected in bronchoalveolar lavage fluid (BALF). Lung tissue histopathology was observed by using H&E, PAS, Masson, and immunohistochemistry staining. qRT-PCR and western blot were applied to analyze key genes and proteins associated with TLR4 and NF-κB signaling pathways.

Results: In OVA-induced asthma mice, YQGB decreased eosinophils and IgE in BALF. YQGB alleviated the OVA-induced inflammatory infiltration and declined IL-4, IL-5, IL-13, Eotaxin, ECP, GM-CSF, LTC4, and LTD4. YQGB attenuated the OVA-induced goblet cell metaplasia and mucus hypersecretion. YQGB mitigated the OVA-induced subepithelial fibrosis and lowered TGF-β1, E-Cadherin, Vimentin, and Fibronectin. YQGB ameliorated the OVA-induced airway smooth muscle thickening and lessened α-SMA and PDGF levels. YQGB reduced the expression of TLR4, MyD88, TRAF6, IκBα, and p65 mRNAs, and IκBα and p-p65 protein levels were also reduced.

Conclusion: YQGB exhibits the anti-asthma effect by reducing airway inflammation and airway remodeling through suppressing TLR4/NF-κB signaling pathway, and is worth promoting clinically.

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来源期刊
CiteScore
6.60
自引率
0.00%
发文量
91
审稿时长
3 months
期刊介绍: JPP keeps pace with new research on how drug action may be optimized by new technologies, and attention is given to understanding and improving drug interactions in the body. At the same time, the journal maintains its established and well-respected core strengths in areas such as pharmaceutics and drug delivery, experimental and clinical pharmacology, biopharmaceutics and drug disposition, and drugs from natural sources. JPP publishes at least one special issue on a topical theme each year.
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