鲁斯可皂苷元干预对铁死亡介导的哮喘小鼠气道炎症的影响OA

Objective To investigate the intervention effect of ruscogenin(Rus)on ovalbumin(OVA)-induced airway inflammation in asthmatic mice and its relationship with ferroptosis.Methods Thirty-six female Balb/c mice were randomly divided into six groups:control(N),model,DMSO,dexamethasone(2 mg/kg),medium-dose Rus(10 mg/kg),and high-dose Rus(15 mg/kg).Except for the control group,all mice were sensitized and challenged with OVA.Sensitization was performed by intraperitoneal injection of OVA(20 μg)combined with aluminum hydroxide(2 mg)on days 1 and 14.The challenge was conducted by aerosol inhalation of 1％OVA for 30 min,three times per week,for a total of 21 days.Drugs were administered intraperitoneally 30 min before each aerosol challenge.Clinical manifestations,including tachypnea,piloerection,and reduced activity,were observed.Lung tissues were examined by HE,Masson,and AB-PAS staining to assess airway inflammation and remodeling.Levels of IL-6,IL-13,and TNF-α were measured by ELISA,while ROS,Fe2+,and MDA were assessed to evaluate oxidative stress.The expression of GPX4,ACSL4,and LOX5 was detected by Western blotting,qPCR,and immunohistochemistry.Results Medium-dose Rus(10 mg/kg)significantly alleviated air-way inflammation,reduced inflammatory cytokines and oxidative stress levels,upregulated GPX4,and downreg-ulated ACSL4 and LOX5.In contrast,high-dose Rus(15 mg/kg)did not show inhibitory effects on certain in-flammatory cytokines.Compared with dexamethasone,Rus exhibited relatively weaker suppression of inflam-matory cytokines but showed consistent improvement in histopathological changes and ferroptosis-related indica-tors.Conclusion Rus improves airway inflammation in asthmatic mice through anti-inflammatory,antioxida-tive,and ferroptosis-regulating mechanisms.Its dose-response effect is not simply monotonic,suggesting the presence of an effective dose window that warrants further investigation.