黄芪甲苷通过S14G-humanin抑制早期生长反应-1介导改善哮喘气道炎症

IF 0.7 4区 材料科学 Q3 Materials Science Materials Express Pub Date : 2023-09-01 DOI:10.1166/mex.2023.2492
Shengnan Zhou, Youlun Li
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引用次数: 0

摘要

本实验探讨黄芪甲苷通过S14G-humanin调节Egr-1在哮喘气道炎症中的作用。选取SD (Sprague Dawley)幼鼠64只。建立大鼠哮喘模型后,随机分为空白对照组、黄芪甲苷组、s14g -人源素组和黄芪甲苷+ s14g -人源素组(联合组)。黄芪甲苷组以黄芪甲苷0.6 mg/kg干预,S14G-Humanin组以50 μ m S14G-Humanin干预,联合组RBSMCs以0.6 mg/kg黄芪甲苷+ 50 μ m S14G-Humanin干预。通过HE染色评估气道反应性和肺组织病理损伤,同时分析支气管肺泡灌洗液(BALF)中炎症细胞、炎症因子和骨髓间充质干细胞(rBMSCs)的行为。与空白对照组相比,黄芪甲苷组、s14g -人源素组和联合组的Penh值升高(P <0.05),病理评分较低,其中联合组评分最低(P <0.05)。黄芪甲苷组、s14g -人源素组和联合用药组大鼠BALF中白细胞、中性粒细胞、嗜酸性粒细胞、巨噬细胞和淋巴细胞数量均降低,以联合用药组最低(P <0.05)。黄芪甲苷组、s14g -人源素组及联合用药组IL-4、IL-6、IL-21均降低,其中联合用药组IL-4、IL-6、IL-21水平最低(P <0.05)。治疗组RBSMCs增殖和迁移能力降低,以联合组最低(P <0.05)。上调S14G-Humanin后,Egr-1 mRNA表达升高(P <0.05)。黄芪甲苷通过调节S14G-Humanin的表达,减少炎症细胞和炎症因子,增加Egr-1的表达。
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Astragaloside improves asthmatic airway inflammation mediated by inhibition of early growth response-1 through S14G-humanin
In this experiment, we explored the role of astragaloside in regulating Egr-1 through S14G-humanin on asthmatic airway inflammation. 64 juvenile Sprague Dawley (SD) rats were selected. After establishing rat asthma model, they were assigned into blank control group, astragaloside group, S14G-Humanin group and astragaloside+S14G-Humanin group (combined group). Astragaloside group was intervened with astragaloside II 0.6 mg/kg, S14G-Humanin group was intervened with 50 μ m S14G-Humanin, combined group RBSMCs were treated with astragaloside II 0.6 mg/kg and 50 μ M S14G-Humaninn. Airway responsiveness was assessed and pathological damage of lung tissue was assessed by HE staining along with analysis of inflammatory cells in bronchoalveolar lavage fluid (BALF), inflammatory cytokines and bone-marrow derived mesenchymal stem cells (rBMSCs) behaviors. Compared to blank control, the Penh values of astragaloside group, S14G-Humanin group and combination group were increased ( P <0.05) and pathological scores were lower with the lowest score in combined group (all P <0.05). The number of white blood cells, neutrophils, eosinophils, macrophages and lymphocytes in BALF of rats in astragaloside group, S14G-Humanin group and combination group were decreased, with the lowest number in combination group ( P <0.05). In addition, IL-4, IL-6, and IL-21 in astragaloside group, S14G-Humanin group and combination group were reduced, with the lowest levels in combination group ( P <0.05). RBSMCs proliferation and migration ability in treatment group was reduced with the lowest in combination group ( P <0.05). After up-regulating S14G-Humanin, Egr-1 mRNA expression was elevated ( P <0.05). Astragaloside can reduce inflammatory cells and inflammatory cytokines and increase the expression of Egr-1 by regulating S14G-Humanin expression.
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Materials Express
Materials Express NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
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