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Aim:To study the effect of honokiol on arterial thrombosis and endothelial cells.Methods:Rabbit platelet aggregation was performed with Born’s turbid method.Thrombosis was produced by the endothelial injury stimulated with electric current.Rat aortic endothelial cells(RAEC)were cultured and cell viability was assessedusing the MTT assay.Nitric oxide(NO)concentrations in serum-free media ofRAEC were determined using the kinetic cadmium-reduction method.The stablemetabolite prostacyclin was measured in serum-free media of RAEC byradioimmunoassay.Results:Honokiol(37.6-376 lamol/L)decreased rabbit plate-let aggregation in vitro in a concentration-dependent manner,while intravenouslyinjection of honokiol(0.12-12 μg/kg)significantly inhibited rabbit platelet aggre-gation induced by collagen ex vivo.In the electrical current-stimulated carotidthrombosis model in rats,honokiol(5-50 μg/kg,iv)prolonged the thrombus oc-clusion time in a does-dependent manner.In vitro honokiol(0.376-37.6 μmol/L)effectively protected cultured RAEC against oxidized low density lipoprotein(ox-LDL )injury,and significantly increased 6-keto-PGF_(1α)(the stable metabolite ofprostacyclin)in serum-free media of RAEC.Honokiol also increased NO level inRAEC serum-free medium at a lower concentration range(0.0376-0.376 μmol/L),but honokiol 3.76 μmol/L decreased NO level.Conclusion:Honokiol is a potentarterial thrombosis inhibitor.Endothelial cell protection and the stimulation ofprostacyclin release may be its main anti-thrombosis mechanism.Stimulation ofNO release in endothelial cells may play a role,but it is not a key factor.
Aim:To study the effect of honokiol on arterial thrombosis and endothelial cells.Methods:Rabbit platelet aggregation was performed with Born’s 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 stablemetabolite prostacyclin was measured in serum-free media of RAEC byradioimmunoassay.Results:Honokiol(37.6-376 Lamol/L)decreased rabbit plate-let aggregation in vitro in a concentration-dependent manner,while intravenouslyinjection of honokiol(0.12-12 μg/kg)significantly inhibited rabbit platelet aggre-gation induced by collagen ex vivo.In the electrical current-stimulated Carotid thrombosis model in rats,honokiol (5-50 μg/kg,iv) prolonged the thrombus oc-clusion time in a does-dependent manner.In vitro honokiol (0.376-37.6 μmol/L )effectively protected cultured RAEC against oxidized low density lipoprotein(ox-LDL)injury, and significantly increased 6-keto-PGF_(1α)(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 μmol/L),but honokiol 3.76 μmol/L decreased NO level.Conclusion:Honokiol is a potentarterial thrombosis inhibitor.Endothelial cell protection and the stimulation of prostacyclin release may be its main anti-thrombosis mechanism.Stimulation ofNO release in endothelial cells may play a role,but it is not a key factor.