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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
- Kim, Hye Yoom, Oh, Hyuncheol, Li, Xiang, Cho, Kyung Woo, Kang, Dae Gill, Lee, Ho Sub
- Journal of ethnopharmacology 2011 v.133 no.2 pp. 315-323
- 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
- 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.