Preclinical study demonstrates that Ahiflower oil reduces lipids and inhibits thrombosis in mouse models, highlighting its potential as a plant-based omega-3 therapy.
Hyperlipidemia is closely associated with endothelial dysfunction and thrombosis. Ahiflower oil is rich in omega-3 polyunsaturated fatty acids (stearidonic acid and α-linolenic acid) and contains the omega-6 fatty acid γ-linolenic acid. We investigated the beneficial effects of Ahiflower oil against hyperlipidemia and thrombosis using both in vitro and in vivo models. In tumor necrosis factor alpha–stimulated human umbilical vein endothelial cells, Ahiflower oil reduced ICAM-1 and VCAM-1 expression and thromboxane B2 release, while increasing eNOS expression and nitric oxide production. The in vivo efficacy was evaluated in three mouse models: high-fat diet-induced hyperlipidemia, poloxamer 407-induced acute hyperlipidemia, and carrageenan-induced inflammation-driven thrombosis. In the high-fat diet model, mice were fed a high-fat diet (60% kcal fat) for 12 weeks; in the poloxamer-407 and carrageenan models, acute hyperlipidemia and thrombosis were induced by a single intraperitoneal injection of poloxamer-407 (300 mg/kg) or carrageenan (50 mg/kg), respectively. In high-fat diet-fed mice, Ahiflower oil modulated aortic adhesion-related gene expression, prolonged tail-bleeding time, and lowered plasma lipid and liver enzyme levels; in poloxamer-407-induced acute hyperlipidemia, Ahiflower oil reduced platelet aggregation and lowered plasma lipid and liver enzyme levels. In carrageenan-induced thrombosis, Ahiflower oil suppressed endothelial activation and platelet aggregation without altering lipid profiles. These results suggest that Ahiflower oil may be a promising plant-derived omega-3 candidate for mitigating endothelial dysfunction and thrombotic risk under hyperlipidemic and inflammatory conditions.
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Oh et al. (2026) studied this question.
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