Objective: Asthma is a very common airway inflammatory disease for which the existing drug therapy options are insufficient. In this study, we explored the mechanisms underlying the anti-inflammatory potential of Sarsapogenin (SG) and its combination with Fluticasone (FC) in ovalbumin (OVA)-induced allergic asthma in mice.Methods: In a standard experimental model, asthma in mice was sensitized and challenged by OVA. The mice were treated with SG and SG + FC during OVA challenge. At the completion, lung weight, inflammatory cell count in bronchoalveolar lavage fluid (BALF), serum cytokines levels, immunoglobulin E (IgE) levels, lung nitrate/nitrite (NO) levels, and lung tissue oxidative stress biomarkers were determined. Histopathological evaluation of the lung tissue was also performed.Key findings: Treatment of mice with SG and SG + FC combination intensely diminished the trafficking of total and differential inflammatory cells count into BALF. SG and SG + FC administration significantly reduced the production of inflammatory cytokines, serum IgE levels and restoration of antioxidant stress markers. Histopathological analysis of lung samples effectually weakened bronchial inflammation and mucus production in the lung with a significant reduction in inflammation and mucus score.Conclusion: Our study results suggested that SG and SG + FC effectively reduced allergic airway inflammation via inhibiting pro-inflammatory cytokines, NO expressions and oxidative stress parameters. So, it could be used as a therapeutic potential agent for the treatment of asthma by decreasing its dose in combination with FC to avoid the chronic adverse effects of FC.

中文翻译：

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Sarsasapogenin和Fluticasone的组合可减轻小鼠哮喘模型中卵白蛋白引起的气道炎症。

目的：哮喘是一种非常常见的气道炎性疾病，其现有的药物治疗方案不足。在这项研究中，我们探索了Sarsapogenin（SG）及其与氟替卡松（FC）联合使用在卵白蛋白（OVA）诱发的小鼠过敏性哮喘中潜在的抗炎机制。方法：在标准实验模型中，小鼠哮喘被OVA敏化和挑战。在OVA攻击期间，用SG和SG + FC治疗小鼠。在完成时，确定肺重量，支气管肺泡灌洗液（BALF）中的炎症细胞计数，血清细胞因子水平，免疫球蛋白E（IgE）水平，硝酸盐/亚硝酸盐（NO）水平以及肺组织氧化应激生物标志物。还进行了肺组织的组织病理学评估。主要发现：用SG和SG + FC组合治疗小鼠大大减少了向BALF转运总和差异性炎症细胞的数量。SG和SG + FC的给药显着降低了炎症细胞因子的产生，血清IgE水平和抗氧化应激指标的恢复。肺样品的组织病理学分析有效减弱了肺中的支气管炎症和粘液生成，并显着降低了炎症和粘液评分。结论：我们的研究结果表明，SG和SG + FC通过抑制促炎性细胞因子有效减少了过敏性气道炎症。表达式和氧化应激参数。因此，通过降低其与FC的剂量以避免FC的慢性副作用，可以将其用作治疗哮喘的潜在治疗剂。