Protective effect of salidroside on lung injury in mice with Poly(I:C)-Induced viral pneumonia based on the TLR4/MyD88/NF-κB signaling pathway

This study aimed to explore the protective effect of salidroside on lung injury in a mouse model of viral pneumonia (VP), and comprehensively elucidating its potential underlying mechanisms. This study successfully established a VP model in mice by intratracheal instillation of Poly (I:C). Mice were divided into different groups, including the control group, model group, low, medium, and high dose treatment groups of salidroside, and positive control group. Lung injury was evaluated by measuring protein levels in lung wet/dry weight ratio; using H&E staining technology to visually observe the pathological changes in lung tissue; using ELISA to detect levels of inflammatory cytokines; measuring oxidative stress markers in lung tissue; and utilizing Western blot to analyze the expression of signaling pathway related proteins. Compared to the model group, salidroside showed better lung protective effects as revealed by significantly reduced lung wet/dry weight ratio, inflammation, and oxidative stress. Salidroside also inhibited the activation of related TLR4/MyD88/NF-κB signaling pathways. Among all dose groups, the high-dose group showed the most significant lung protective effect. Salidroside exerts protective effects by inhibiting TLR4/MyD88/NF-κB pathway activation, consequently reducing inflammation and oxidative stress markers and providing a solid theoretical basis for the potential clinical application of this drug in the treatment of VP.