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, 26 (9), 1063-8

Honokiol Inhibits Arterial Thrombosis Through Endothelial Cell Protection and Stimulation of Prostacyclin

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Honokiol Inhibits Arterial Thrombosis Through Endothelial Cell Protection and Stimulation of Prostacyclin

He Hu et al. Acta Pharmacol Sin.

Abstract

Aim: To study the effect of honokiol on arterial thrombosis and endothelial cells.

Methods: Rabbit platelet aggregation was performed with Borns turbid method. Thrombosis was produced by the endothelial injury stimulated with electric current. Rat aortic endothelial cells (RAEC) were cultured and cell viability was assessed using the MTT assay. Nitric oxide (NO) concentrations in serum-free media of RAEC were determined using the kinetic cadmium-reduction method. The stable metabolite prostacyclin was measured in serum-free media of RAEC by radioimmunoassay.

Results: Honokiol (37.6-376 micromol/L) decreased rabbit platelet aggregation in vitro in a concentration-dependent manner, while intravenously injection of honokiol (0.12-12 microg/kg) significantly inhibited rabbit platelet aggregation induced by collagen ex vivo. In the electrical current-stimulated carotid thrombosis model in rats, honokiol (5-50 microg/kg, iv) prolonged the thrombus occlusion time in a does-dependent manner. In vitro honokiol (0.376-37.6 micromol/L) effectively protected cultured RAEC against oxidized low density lipoprotein (ox-LDL) injury, and significantly increased 6-keto-PGF1alpha (the stable metabolite of prostacyclin) in serum-free media of RAEC. Honokiol also increased NO level in RAEC serum-free medium at a lower concentration range (0.0376-0.376 micromol/L), but honokiol 3.76 micromol/L decreased NO level.

Conclusion: Honokiol is a potent arterial thrombosis inhibitor. Endothelial cell protection and the stimulation of prostacyclin release may be its main anti-thrombosis mechanism. Stimulation of NO release in endothelial cells may play a role, but it is not a key factor.

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