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Ethanol extract of seeds of Oenothera odorata induces vasorelaxation via endothelium-dependent NO-cGMP signaling through activation of Akt-eNOS-sGC pathway

Author:
Kim, Hye Yoom, Oh, Hyuncheol, Li, Xiang, Cho, Kyung Woo, Kang, Dae Gill, Lee, Ho Sub
Source:
Journal of ethnopharmacology 2011 v.133 no.2 pp. 315-323
ISSN:
0378-8741
Subject:
biochemical pathways, calcium, carotid arteries, cyclic GMP, endothelium, enzyme inhibitors, ethanol, glibenclamide, guanosine monophosphate, guanylate cyclase, nitric oxide synthase, protein kinases, rats, seed extracts, signal transduction, smooth muscle, tea, vasodilation
Abstract:
AIM OF STUDY: The vasorelaxant effect of ethanol extract of seeds of Oenothera odorata (Onagraceae) (one species of evening primroses) (ESOO) and its mechanisms involved were defined. MATERIALS AND METHODS: Changes in vascular tension, guanosine 3′,5′-cyclic monophosphate (cGMP) levels, and Akt expression were measured in carotid arterial rings from rats. Seeds of Oenothera odorata were extracted with ethanol (94%) and the extract was filtered, concentrated and stored at −70°C. RESULTS: ESOO relaxed endothelium-intact, but not endothelium-denuded, carotid arterial rings in a concentration-dependent manner. Similarly, ESOO increased cGMP levels of the carotid arterial rings. Pretreatment of endothelium-intact arterial rings with L-NAME, an inhibitor of nitric oxide synthase (NOS), or ODQ, an inhibitor of soluble guanylyl cyclase (sGC), blocked the ESOO-induced vasorelaxation and increase in cGMP levels. Nominally Ca²⁺-free but not L-typed Ca²⁺ channel inhibition attenuated the ESOO-induced vasorelaxation. Thapsigargin, Gd³⁺, and 2-aminoethyl diphenylborinate, modulators of store-operated Ca²⁺ entry (SOCE), significantly attenuated the ESOO-induced vasorelaxation and increase in cGMP levels. Further, wortmannin, an inhibitor of Akt, attenuated the ESOO-induced vasorelaxation and increases in cGMP levels and phosphorylated Akt2 expression. K⁺ channel blockade with TEA, 4-aminopyridine, and glibenclamide attenuated the ESOO-induced vascular relaxation. CONCLUSION: Taken together, the present study demonstrates that ESOO relaxes vascular smooth muscle via endothelium-dependent NO-cGMP signaling through activation of the Akt-eNOS-sGC pathway.
Agid:
577898