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KMID : 0620720140200030216
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Natural Product Sciences
2014 Volume.20 No. 3 p.216 ~ p.225
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Ethylacetate Fraction of Rubus coreanum Causes Vascular Relaxation and Hypotensive Action
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Hong Soon-Pyo
Choi Mee-Sung
Lim Dong-Yoon
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Abstract
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The present study was designed to investigate whether ethylacetate (EtOAc) fraction extracted from Rubus coreanum affect the contractility of the isolated thoracic aortic strips and blood pressure of normotensive rats. The EtOAc fraction (400 μg/mL) significantly depressed both phenylephrine (PE, 10 μM)- and high K+ (56 mM)-induced contractile responses of the isolated thoracic aortic strips in a concentration-dependent fashion. In the simultaneous presence of L-NAME (an inhibitor of NO synthase, 300 μM) and EtOAc (400 μg/mL), both PE- and high K+-induced contractile responses were recovered to the corresponding control level in comparison with inhibition of EtOAc-treatment alone. Moreover, in the simultaneous presence of EtOAc after pretreatment with 0.4% CHAPS, both PE- and high K+-induced contractile responses were recovered to the corresponding control level compared to the inhibitory response of EtOAc-treatment alone. Also, in anesthetized rats, EtOAc fraction (0.3~3.0 mg/kg) injected into a femoral vein dose-dependently produced depressor responses. This hypotensive action of EtOAc fraction was greatly inhibited after treatment with phentolamine (1 mg/kg), chlorisondamine (1 mg/kg), L-NAME (3 mg/kg/30 min) or sodium nitroprusside (30 μg/kg/30 min). Intravenous infusion of EtOAc fraction (1.0~10.0 mg/kg/30 min) markedly inhibited norepinehrine-induced pressor responses. Taken together, these results demostrate that EtOAc causes vascular relaxation in the isolated rat thoracic aortic strips as well as hypotensive action in anesthetized rats. These vasorelaxation and hypotension of EtOAc seem to be mediated at least by the increased NO production through the activation of NO synthase of vascular endothelium, and the inhibitory adrenergic modulation.
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KEYWORD
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Rubus coreanum, Bokboonja, Ethylacetate, EtOAc, fraction, Vasorelaxation, Hypotension, Adrenergic α1-receptors blockade, Activation of NO synthase
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