Ruscogenin alleviates LPS-induced pulmonary endothelial cell apoptosis by suppressing TLR4 signaling

Publication date: May 2020Source: Biomedicine & Pharmacotherapy, Volume 125Author(s): Yunhao Wu, Yuwei Wang, Shuaishuai Gong, Jiahui Tang, Jiazhi Zhang, Fang Li, Boyang Yu, Yuanyuan Zhang, Junping KouAbstractAcute lung injury (ALI) or its most advanced form, acute respiratory distress syndrome (ARDS) is a severe inflammatory pulmonary process triggered by varieties of pathophysiological factors, among which apoptosis of pulmonary endothelial cells plays a critical role in the progression of ALI/ARDS. Ruscogenin (RUS) has been found to exert significant protective effect on ALI induced by lipopolysaccharides (LPS), but there is little information about its role in LPS-induced pulmonary endothelial cell apoptosis. The aim of the present study was to investigate the underlying mechanism in which RUS attenuates LPS-induced pulmonary endothelial cell apoptosis. Mice were challenged with LPS (5 mg/kg) by intratracheal instillation for 24 h to induce apoptosis of pulmonary endothelial cells in model group. RUS (three doses: 0.1, 0.3, and 1 mg/kg) was administrated orally 1 h prior to LPS challenge. The results showed that RUS could attenuate LPS-induced lung injury and pulmonary endothelial apoptosis significantly. And we observed that RUS inhibited the activation of TLR4/MYD88/NF-κB pathway in pulmonary endothelium after LPS treatment. In murine lung vascular endothelial cells (MLECs) we further confirmed that RUS (1 μmol/L) markedly ameliorated MLECs apoptosis by suppr...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research