Mechanism of Saikosaponin D on Lipopolysaccharide-Induced Acute Lung Injury in Neonatal Rats

Abstract

This study investigates the mechanism of saikosaponin D on lipopolysaccharide (LPS) aspiration pneumonia in neonatal rats. Inhalation lung injury model was constructed and rats were assigned into control group, model group, saikosaponin D (5, 10 or 20 mg/kg) group and dexamethasone 2 mg/kg group (positive control group). The dry and wet mass ratio of lung tissue was measured by wet and dry method. Superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), IL-6, IL-1β and TNF-α were measured by ELISA. HMGB1, TLR4 and p-NF-κB p65 protein expressions were detected by Western blot. Compared with control group, model group had significantly higher wet and dry mass ratio of lung tissue, lower SOD and GSH contents, higher MDA content, higher IL-6/IL-1β/TNF-α levels, higher HMGB1 and TLR4 levels and higher p-NF-κB p65 to NF-κB p65 ratio (P <0.05). Compared with model group, dry and wet mass ratios of lungs in saikosaponin D groups and dexamethasone group were reduced, SOD and GSH contents were increased, and MDA contents were reduced. Meanwhile, IL-6/IL-1β/TNF-α levels were reduced and HMGB1 and TLR4 levels and p-NF-κB p65 ratio were reduced (P < 0.05). In conclusion, saikosaponin D inhibited release of inflammatory factors, improved oxidative stress and HMGB1/TLR4/NF-κB signaling in LPS-induced inhalational lung injury.