Ginsenoside compound K attenuates hypoxic pulmonary hypertension endothelial injury by suppressing POSTN-TrkB-mediated endothelial-mesenchymal transition.

OBJECTIVES

Hypoxia-induced pulmonary hypertension (HPH) involves endothelial injury, vascular inflammation, and endothelial-mesenchymal transition (EndMT). Ginsenoside compound K (CK) has anti-inflammatory and vascular-protective properties, but its role in HPH remains unclear.

METHODS

Hypoxia-stimulated human pulmonary artery endothelial cells and chronic hypoxia-induced PH rats were used to assess the protective effects and mechanisms of CK.

KEY FINDINGS: CK reduced MCP-1, BMP2, and RANKL expression, indicating attenuation of endothelial injury and pro-calcification responses. CK also dose-dependently reversed hypoxia-induced EndMT, shown by decreased vimentin and restored CD31 expression in vitro and in vivo. In HPH rats, intraperitoneal CK improved pulmonary hemodynamics, reduced right ventricular hypertrophy, and alleviated endothelial damage. Mechanistically, CK inhibited POSTN expression, downregulated TrkB, and suppressed recombinant POSTN-induced TGF-β/Smad2/3/Snail signaling.

CONCLUSIONS

CK protects against hypoxia-induced endothelial injury and vascular remodeling by inhibiting the POSTN-dependent EndMT pathway, suggesting its preventive potential for HPH-related cardiovascular complications.