Xuebijing Injection Ameliorates H2S-Induced Acute Respiratory Distress Syndrome by Promoting Claudin-5 Expression

• 作者: GENG Ping LING Bing-yu ZHANG Hong-liang XIONG Jia-li WANG Ying YU Fen TAN Ding-yu XU Ji-yang WANG Hui-hui
• 来源期刊: 中国结合医学杂志（英文版）
• 年，卷（期）: 2022,（2）
• 所属期刊栏目: Original Articles
• 页码范围: 116-123
• 页数: 8页
• 语种: 英文
• DOI: 10.1007/s11655-021-3344-3

摘要

Objective:To investigate the protective effects and underlying mechanisms of Xuebijing Injection (XBJ) on the lung endothelial barrier in hydrogen sulfide (H2S)-induced acute respiratory distress syndrome (ARDS).Methods:Sprague-Dawley rats were exposed to H2S (300 ppm) to establish ARDS model,while human pulmonary microvascular endothelial cells (HPMECs) were incubated with NaHS(a H2S donor,500 μ mol/L) to establish cell model.H2S and XBJ were concurrently administered to the rat and cell models.Lung hematoxylin and eosin staining,immunohistochemistry,transmission electron microscopy and wet/dry ratio measurement were used to confirm ARDS induced by H2S in vivo.The expression levels of claudin-5,phosphorylated protein kinase B (p-AKT)/t-AKT and p-forkhead box transcription factor O1(FoxO1)/t-FoxO1 in vivo and in vitro were also assessed.Paracellular permeability and transepithelial electrical resistance (TEER) were measured to evaluate endothelial barrier function in the cell model.Results:The morphological investigation showed that XBJ attenuated H2S-induced ARDS in rats.XBJ significantly ameliorated both the reduction in TEER and the increased paracellular permeability observed in NaHS-treated HPMECs (P＜0.05).The protective effects of XBJ were blocked by LY294002,a phosphatidylinositol 3-kinase(PI3K)/AKT/FoxO1 pathway antagonist (P＜0.05).Furthermore,XBJ promoted the expression of claudin-5 and increased the levels of p-AKT and p-FoxO1 in vivo and in vitro (P＜0.05).Conclusion:XBJ ameliorated H2S-induced ARDS by promoting claudin-5 expression via the PI3K/AKT/FoxO1 signaling pathway.