An ethanolic extract of Lindera obtusiloba stems causes NO-mediated endothelium-dependent relaxations in rat aortic rings and prevents angiotensin II-induced hypertension and endothelial dysfunction in rats
- An ethanolic extract of Lindera obtusiloba stems causes NO-mediated endothelium-dependent relaxations in rat aortic rings and prevents angiotensin II-induced hypertension and endothelial dysfunction in rats
- 이정옥; 옥민호; 정상훈; 박동현; Auger Cyril; 김경락; 이승우; Schini-Kerth Valerie
- Lindera obtusiloba; Endothelium-dependent relaxation; Endothelial NO synthase; Angiotensin II; Hypertension
- Issue Date
- Naunyn-schmiedebergs archives of pharmacology
- VOL 383, NO 6, 635-645
- Lindera obtusiloba is a medical herb traditionally
used in Asia for the improvement of blood circulation,
treatment of inflammation, and prevention of liver damage.
The possibility that L. obtusiloba affects vascular reactivity
remains to be examined. Therefore, the aim of the present
study was to evaluate both the in vitro and in vivo vascular
effects of an ethanolic extract of L. obtusiloba stems (LOE).
Vascular reactivity was assessed in organ chambers using
rat aortic rings and the activation of endothelial NO
synthase (eNOS) in cultured bovine aortic endothelial cells.
LOE induced endothelium-dependent relaxations, which were abolished by inhibitors of nitric oxide synthase
(Nω-nitro-L-arginine) and guanylyl cyclase (1H-[1,2,4] oxadiazolo
[4,3-a] quinoxalin-L-one), significantly reduced by
inhibitors of PI3 kinase (wortmannin and LY294002), and not
affected by inhibitors of cyclooxygenase (indomethacin) and
endothelium-derived hyperpolarizing factor-mediated
responses (charybdotoxin plus apamin). LOE prevented
contractile responses to phenylephrine and angiotensin II in
rings with endothelium, but not in those without endothelium.
LOE caused a concentration-dependent phosphorylation of
Akt at Serine473 and eNOS at Serine1177 in endothelial
cells. Thereafter, the vasoprotective effect of LOE was
investigated in an experimental model of hypertension in
rats. Intake of LOE prevented the angiotensin II-induced
increase in systolic blood pressure, and endothelial dysfunction
to acetylcholine and oxidative stress as assessed using
dihydroethidine in aortic rings. The present findings indicate
that LOE has vasoprotective and antihypertensive properties
most likely by stimulating the endothelial formation of NO
and inhibiting oxidative stress.
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