Quinic acid derivatives from Salicornia herbacea alleviate HMGB1-mediated endothelial dysfunction

• HMGB1 is a critical target for modulating vascular inflammatory responses.
• New caffeoylated quinic acids were isolated from Salicornia herbacea.
• The crude extract exhibited potent inhibition of HMGB1.
• Caffeoylated quinic acids alleviate HMGB1-mediated endothelial dysfunction.
• Caffeoyl quinic acids improved survival rates of CLP-induced septic in vivo models.
• Caffeoyl quinic acids can be commercialized as functional food components.

The high mobility group box 1 protein (HMGB1) has been targeted in the discovery of dietary supplements or medicinal resources to treat vascular inflammatory diseases. Salicornia herbacea has been utilized as a seasoned vegetable, salad, and traditional medicinal resource as well. Two new (1 and 2) and four known (3–6) caffeoylated quinic acids (CQAs) were isolated from the crude extract of S. herbacea exhibiting anti-HMGB1 activity. The isolated CQAs were further evaluated for their potential to ameliorate HMGB1-mediated vascular barrier disruption. Compounds 1, 3, 5, and 6 exerted vascular protective activity against HMGB1-induced inflammatory responses in both cellular and animal models and their mechanisms were also addressed. The active CQAs increased survival rates of cecal ligation and puncture-induced severe septic models to 20–40%. This study may serve the groundwork for commercializing CQAs as functional food components for prevention and treatment of pathogenic conditions related to endothelial hyperpermeability.