Mendelian randomization analysis reveals the mechanism of salidroside in the treatment of eosinophilic asthma

Abstract Introduction: Eosinophilic asthma (EA) is the predominant inflammatory phenotype of asthma commonly found in clinical settings. Salidroside is a phenolic glycoside molecule derived from the rhodiola plant. Furthermore, it possesses the ability to regulate apoptosis, oxidative stress, autophagy, and inflammation. The objective of this study was to assess the impact of salidroside on EA and elucidate its underlying mechanism. Methods The mice with asthma-like symptoms were induced using ovalbumin (OVA) and then treated with salidroside at a dosage of 50mg/kg and dexamethasone at a dosage of 1mg/kg. The effects of salidroside and dexamethasone on IgE and type 2 inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice were investigated using ELISA and qPCR. The online database provided information on the pertinent targets for salidroside-assisted EA treatment. Additionally, mendelian randomization further discovered pertinent targets for salidroside-assisted EA treatment. Results Salidroside demonstrated significant inhibitory effects on the expression levels of IgE and type 2 cytokines (IL-4, IL-5, IL-13, TSLP) in model mice. The KIF3A gene, located next to the IL-4/IL-13 gene, can serve as a potential target for the therapy of EA concerning salidroside. Conclusions Salidroside exhibits potential as a pharmacological intervention for EA.