毛蕊异黄酮对变应性哮喘小鼠气道炎症及气道重塑的影响

Li Huang, Mingjuan Zhang, Jin-rong Xiong
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摘要

背景:本研究旨在构建tdi诱导的小鼠哮喘模型,探讨毛蕊异黄酮对小鼠气道炎症和气道重塑的潜在作用及可能的分子机制。材料与方法:采用ELISA法检测大鼠支气管肺泡灌洗液中血清总IgE水平和炎性细胞因子水平。光学显微镜下观察BALF细胞总数及炎性细胞比例。采用HE法评估和评分各组小鼠肺组织中气管周围和血管周围炎症细胞的浸润情况,采用PAS染色法评估各组小鼠气道上皮杯状细胞比例及气道上皮网状基底膜厚度。WB检测细胞中HMGB1和a-SMA的表达。免疫荧光染色检测16HBEs中HMGB1和a-SMA的表达。结果:毛囊素TDI哮喘小鼠气道高反应性降低,BALF炎症因子和血清总IgE水平降低,气道上皮杯状细胞化生和气道上皮网状基底膜厚度改善,从而降低了TDI- hsa诱导的HMGB1和a-SMA表达上调。结论:在我们的研究中,在tdi诱导的哮喘小鼠模型中,给予抑制AKT激活的药物可以减轻气道炎症和气道重塑。这些发现丰富了目前对毛蕊花素的认识,为今后的研究提供了基础。然而,也存在一些局限性:TDI如何激活AKT信号通路?AKT通路激活后,HMGB1、α-SMA和Collagen-I表达上调的机制尚未完全阐明。
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Effect of Calycosin on Airway Inflammation and Airway Remodeling in Allergic Asthma Mouse Model
Background: This study aimed to construct a TDI-induced mouse model of asthma, and evaluate the potential effects and possible molecular mechanisms of Calycosin on airway inflammation and airway remodeling in mouse model. Material and methods: ELISA method was applied to detect the total serum IgE level and the inflammatory cytokine level in the bronchoalveolar lavage fluid. The total number of cells and the proportion of inflammatory cells in BALF were evaluated under an optical microscope. HE was employed to assess and score the infiltration of peritracheal and perivascular inflammatory cells in lung tissue, and PAS staining was used to assess the proportion of goblet cells in the airway epithelium and the thickness of airway epithelial reticular basement membrane in each group of mice. WB was used to detect the expressions of HMGB1 and a-SMA in cells. Immunofluorescence staining was used to detect the expressions of HMGB1 and a-SMA in 16HBEs. Results: The airway hyperresponsiveness of the Calycosin TDI asthma mice decreased, the inflammatory factors in BALF and the total serum IgE levels decreased, the airway epithelial goblet cell metaplasia and the thickness of the airway epithelial reticular basement membrane were improved, thus reducing the up-regulation of HMGB1 and a-SMA expression of 16HBES induced by TDI-HSA. Conclusion: In our study, in the TDI-induced mouse model of asthma, the administration of drug to inhibit the activation of AKT can reduce airway inflammation and airway remodeling. These findings have enriched the current understanding of Calycosin and provided a basis for future research. However, there are also some limitations: How does TDI activate the AKT signaling pathway? After the activation of the AKT pathway, the mechanism by which the expressions of HMGB1, α-SMA and Collagen-I were up-regulated has not been fully elucidated.
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