Vasorelaxant properties of Vernonia amygdalina ethanol extract and its possible mechanism.

CONTEXT

Vernonia amygdalina Del. (VA) (Asteraceae) is commonly used to treat hypertension in Malaysia.

OBJECTIVE

This study investigates the vasorelaxant mechanism of VA ethanol extract (VAE) and analyzes its tri-step FTIR spectroscopy fingerprint.

MATERIALS AND METHODS

Dried VA leaves were extracted with ethanol through maceration and concentrated using rotary evaporator before freeze-dried. The vasorelaxant activity and the underlying mechanisms of VAE using the cumulative concentration (0.01-2.55 mg/mL at 20-min intervals) were evaluated on aortic rings isolated from Sprague Dawley rats in the presence of antagonists.

RESULTS

The tri-step FTIR spectroscopy showed that VAE contains alkaloids, flavonoids, and saponins. VAE caused the relaxation of pre-contracted aortic rings in the presence and absence of endothelium with EC of 0.057 ± 0.006 and 0.430 ± 0.196 mg/mL, respectively. In the presence of Nω-nitro-l-arginine methyl ester (EC 0.971 ± 0.459 mg/mL), methylene blue (EC 1.203 ± 0.426 mg/mL), indomethacin (EC 2.128 ± 1.218 mg/mL), atropine (EC 0.470 ± 0.325 mg/mL), and propranolol (EC 0.314 ± 0.032 mg/mL), relaxation stimulated by VAE was significantly reduced. VAE acted on potassium channels, with its vasorelaxation effects significantly reduced by tetraethylammonium, 4-aminopyridine, barium chloride, and glibenclamide (EC 0.548 ± 0.184, 0.158 ± 0.012, 0.847 ± 0.342, and 0.304 ± 0.075 mg/mL, respectively). VAE was also found to be active in reducing Ca released from the sarcoplasmic reticulum and blocking calcium channels.

CONCLUSIONS

The vasorelaxation effect of VAE involves upregulation of NO/cGMP and PGI signalling pathways, and modulation of calcium/potassium channels, and muscarinic and β-adrenergic receptor levels.