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

Area of Science:

• Pulmonary Medicine
• Cell Biology
• Pharmacology

Background:

• Hydrogen sulfide (H2S) exposure can induce acute respiratory distress syndrome (ARDS), characterized by lung endothelial barrier dysfunction.
• Investigating therapeutic interventions for H2S-induced ARDS is crucial for improving patient outcomes.

Purpose of the Study:

• To evaluate the protective effects of Xuebijing Injection (XBJ) on the lung endothelial barrier in a model of H2S-induced ARDS.
• To elucidate the underlying molecular mechanisms of XBJ's protective action.

Main Methods:

• ARDS models were established in Sprague-Dawley rats exposed to H2S and in human pulmonary microvascular endothelial cells (HPMECs) treated with NaHS.
• XBJ was administered concurrently with H2S/NaHS.
• Lung histology, wet/dry ratio, immunohistochemistry, transmission electron microscopy, paracellular permeability, and transepithelial electrical resistance (TEER) were assessed. Protein expression levels of claudin-5, AKT, and FoxO1 were quantified.

Main Results:

• XBJ treatment attenuated H2S-induced lung injury in rats and improved endothelial barrier function in HPMECs, evidenced by restored TEER and reduced paracellular permeability.
• XBJ promoted claudin-5 expression and increased phosphorylation of AKT and FoxO1.
• The protective effects of XBJ were diminished by the PI3K/AKT/FoxO1 pathway inhibitor LY294002.

Conclusions:

• Xuebijing Injection demonstrates significant protective effects against H2S-induced ARDS.
• XBJ ameliorates lung endothelial barrier damage by upregulating claudin-5 expression.
• These effects are mediated through the activation of the PI3K/AKT/FoxO1 signaling pathway.