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.
Ginsenoside compound K (CK) reduced markers of endothelial injury and pro-calcification responses in hypoxia-stimulated human pulmonary artery endothelial cells.
CK dose-dependently reversed hypoxia-induced endothelial-mesenchymal transition (EndMT) in vitro and in vivo.
In rats with chronic hypoxia-induced pulmonary hypertension, intraperitoneal CK improved pulmonary hemodynamics, reduced right ventricular hypertrophy, and alleviated endothelial damage.
CK inhibited POSTN expression and downregulated its putative receptor TrkB.
CK suppressed recombinant POSTN-induced TGF-β/Smad2/3/Snail signaling.
The authors conclude that CK protects against hypoxia-induced endothelial injury and vascular remodeling by inhibiting POSTN-dependent EndMT, suggesting preventive potential for HPH-related cardiovascular complications.
This study looked at whether ginsenoside compound K (CK), a compound derived from ginseng with known anti-inflammatory and blood-vessel-protective properties, could help in hypoxia-induced pulmonary hypertension, a condition where low oxygen leads to high blood pressure in the lungs' arteries. The researchers used human lung artery cells exposed to low oxygen and rats kept in chronic low-oxygen conditions. CK reduced markers of inflammation and blood vessel cell injury, and it reversed a process called endothelial-mesenchymal transition, in which cells lining blood vessels lose their normal identity and take on features that contribute to vessel wall thickening. In the rats, CK given by injection improved lung blood pressure measures, reduced enlargement of the right side of the heart, and lessened damage to the vessel lining. The compound appeared to act by lowering periostin (POSTN) and its receptor TrkB, and by dampening a downstream TGF-β/Smad2/3/Snail signaling pathway. This research suggests CK might be a candidate for preventing blood vessel damage in hypoxia-related pulmonary hypertension. However, the work was done in cultured cells and rats, so it remains unknown whether similar effects would occur or be safe in people.
Ren J, Wang S, Ye C, Fan X, He R. (2026). Ginsenoside compound K attenuates hypoxic pulmonary hypertension endothelial injury by suppressing POSTN-TrkB-mediated endothelial-mesenchymal transition.. The Journal of pharmacy and pharmacology. https://doi.org/10.1093/jpp/rgag125