Conclusion
SH relieved VILI by inhibiting the ROS-mediated JNK pathway.
Methods
The male mice VILI model was established by high tidal volume ventilation. The cell model was established by performing cell stretch (CS) experiments on murine respiratory epithelial cells MLE-15. In addition, the JNK activator Anisomycin and JNK inhibitor SP600125 were used on VILI mice and CS-treated cells.
Purpose
Ventilator-induced lung injury (VILI) is a serious complication of mechanical ventilation (MV) that increases morbidity and mortality of patients receiving ventilator treatment. This study aimed to reveal the molecular mechanism of sodium houttuyfonate (SH) on VILI. Materials and
Results
VILI modeling damaged the structural integrity, increased apoptosis and wet-to-dry (W/D) ratio, enhanced the levels of inflammatory factors, reactive oxygen species (ROS) and malonaldehyde (MDA), and activated JNK pathway in lung tissues. SH gavage alleviated lung injury, decreased apoptosis and W/D ratio, and reduced levels of inflammatory factors, ROS and MDA, and p-JNK/JNK expression of lung tissues in VILI mice. However, activation of JNK wiped the protective effect of SH on VILI. Contrary results were found in experiments with JNK inhibitor SP600125.