• Yi Liu, Gang Tang, and Jinyu Li.
• Department of Anesthesiology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.
• Yonsei Med. J. 2021 Jun 1; 62 (6): 545-554.

PurposeVentilator-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 MethodsThe 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.ResultsVILI 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.ConclusionSH relieved VILI by inhibiting the ROS-mediated JNK pathway.© Copyright: Yonsei University College of Medicine 2021.

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