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Vascular Relaxation by the Methanol Extract of <i>Sorbus</i> Cortex <i>via</i> NO-cGMP Pathway
Kang, Dae Gill,Lee, Jun Kyoung,Choi, Deok Ho,Sohn, Eun Jin,Moon, Mi Kyoung,Lee, Ho Sub Pharmaceutical Society of Japan 2005 BIOLOGICAL & PHARMACEUTICAL BULLETIN Vol.28 No.5
<P>The methanol extract of <I>Sorbus commixta</I> cortex (MSC) induced relaxation of the phenylephrine-precontracted aorta in a dose-dependent manner, which was disappeared by removal of functional endothelium. Pretreatment of the aortic tissues with <I>N</I><SUP>G</SUP>-nitro-<SMALL>L</SMALL>-arginine methyl ester (<SMALL>L</SMALL>-NAME), methylene blue, or 1<I>H</I>-[1,2,4]-oxadiazole-[4,3-α]-quinoxalin-1-one (ODQ) inhibited the vascular relaxation induced by MSC. MSC-induced vascular relaxations were also markedly attenuated by addition of verapamil or diltiazem, while the relaxant effect of MSC was not blocked by pretreatment with indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, or propranolol, respectively. Incubation of endothelium-intact carotid arteries or of human umbilical vein endothelial cells (HUVECs) with MSC increased the production of guanosine 3′,5′-cyclic monophosphate (cGMP). Moreover, MSC-induced cGMP production was effect was blocked by pretreatment with <SMALL>L</SMALL>-NAME or ODQ. These results suggest that MSC dilates vascular smooth muscle <I>via</I> endothelium-dependent nitric oxide-cGMP signaling pathway, possible involvement of L-type Ca<SUP>2+</SUP> channel.</P>
Kang, Dae Gill,Sohn, Eun Jin,Lee, An Sook,Kim, Jin Sook,Lee, Dae Ho,Lee, Ho Sub Institute for Advanced Research in Asian Science a 2007 The American journal of Chinese medicine Vol.35 No.2
<P>Feeding high fructose (Frc) to rats induces a moderate increase in blood pressure, which is associated with insulin resistance. The present study was designed to evaluate the effect of the methanol extract of Sorbus commixta cortex (MSC) on vascular inflammation in a rat model of the metabolic syndrome induced by a high Frc-diet. Male Sprague-Dawley rats were divided into 4 groups and treated for 7 weeks as follows: 1) control, 2) high Frc-diet group, 3) Frc/MSC1 group; high Frc-diet group treated with MSC (100 mg/kg/day), and 4) Frc/MSC2 group; high Frc-diet group treated with MSC (200 mg/kg/day). High Frc-induced decreases of the expression level of aortic endothelial nitric oxide synthase (ecNOS) while the production of cyclic GMP (cGMP) was restored by treatment with MSC. On the contrary, increases of the expression level of endothelin-1 (ET-1) in the aorta, the transcription factor, the cytokine related with vascular inflammation, and the adhesion molecules were suppressed by MSC treatment. Moreover, MSC treatment was shown to lessen the thickening noted in the aortic intima and media of the high Frc-diet group. Our findings suggest that MSC may have an anti-vascular inflammatory effect on rats with a high Frc-induced metabolic syndrome.</P>
Kang Dae-Gill,Sohn Eun-Jin,Choi Deok-Ho,Lee Seung-Ju,Lee Ho-Sub The Physiological Society of Korean Medicine and T 2006 동의생리병리학회지 Vol.20 No.1
A pharmacological inhibition of nitric oxide synthase (NOS) in rats produces vasoconstriction, renal dysfunction, and hypertension. The present study was aimed at investigating whether the methanol extract of Serous commixta cortex (MSC) ameliorates $N^G$-nitro-L-arginine methylester (L-NAME) induced hypertension in rats. Treatment of rats with L-NAME (10 mg/kg/day in drinking water, 5 weeks) caused a sustained increase in systolic blood pressure (SBP). Administration of MSC (100 or 200 mg/kg/day, p.o) significantly lowered the SBP in the L-NAME-treated rats and this effect was maintained throughout the whole experimental period. Moreover, ecNOS expression in aorta and kidney tissue from L-NAME treated rats was significantly restored dy administration of MSC. Furthermore, the impairment of acetylcholine (ACh)-induced relaxation of aortic rings in the L-NAME treated rats was reversed dy administering of MSC. The renal functional parameters including urinary volume, sodium excretion, and creatinine clearance (Ccr) were also restored by administering MSC. Taken together, the present study suggeststhat MSC prevents the increase in SBP in rats with L-NAME-induced hypertension, which may result from the up-regulation of the vascular and renal ecNOS/No system.
Kang, Dae Gill,Moon, Mi Kyoung,Lee, An Sook,Kwon, Tae Oh,Kim, Jin Sook,Lee, Ho Sub Pharmaceutical Society of Japan 2007 Biological & pharmaceutical bulletin Vol.30 No.9
<P>Cornuside is a bisiridoid glucoside compound isolated from the fruit of <I>Cornus officinalis</I> S<SMALL>IEB</SMALL>. <I>et</I> Z<SMALL>UCC</SMALL>. The present study was designed to examine the effects of cornuside on expression levels of cytokine-induced proinflammatory and adhesion molecules in the human umbilical vein endothelial cells (HUVECs). Cornuside treatment attenuated tumor necrosis factor-α (TNF-α)-induced nuclear factor-kappa B (NF-κB) p65 translocation in HUVECs. In addition, cornuside suppressed the expression levels of endothelial cell adhesion molecules including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) induced by TNF-α. TNF-α-induced monocyte chemoattractant protein 1 (MCP-1) expression was also attenuated by treatment of cornuside. These inhibitory effects of cornuside on proinflammatory and adhesion molecules were not due to decreased HUVEC viability as assessed by MTT test. Taken together, the present study suggests that cornuside suppresses expression levels of cytokine-induced proinflammatory and adhesion molecules in the human endothelial cells.</P>
Kang, Dae-Gill,Sohn, Eun-Jin,Kim, Jin-Sook,Lee, Yun-Jung,Moon, Mi-Kyoung,Lee, An-Sook,An, Jun-Seok,Lee, Ho-Sub The Physiological Society of Korean Medicine and T 2006 동의생리병리학회지 Vol.20 No.5
Hypercholesterolemia is a pivotal pathogenic factor for the development and maintenance of atherosclerosis. The present study was designed to evaluate whether the methanol extract of Sorbus commixta cortex (MSC) restores vascular dysfunction in association with the aortic expressions of proinflarnmatory and adhesion molecules in high cholesterol (HC) diet-rats. Chronic treatment with low (100 mg/kg/day) or high doses (200 mg/kg/day) of MSC lowered the increase in plasma levels of triglyceride (TG) and low-density lipoprotein (LDL) cholesterol induced by a cholesterol-enriched diet without affecting on the plasma level of high density lipoprotein (HDL)-cholesterol. Vascular tone attenuated in the HC-diet rats was restored by administration with MSC. Treatment with MSC also suppressed the HC-induced increase in the monocyte chemoattractant protein-1 (MCP-1) and nuclear factor-$_K$B (NF-$_K$B) p65 expressions as well as expressions levels of adhesion molecules including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (ICAM-1), and E-selectin in aorta. The present study also showed that MSC inhibited the HC-mediated induction of ET-1 and ACE expression. In histopathological examination, aortic segments in the HC-diet rat revealed thickening intima and media, which were blocked by administration with MSC. Taken together, MSC could suppress the development of atherosclerosis in the HC-diet rat model through the inhibition of the aortic expression levels of pro-inflammatory and adhesion molecules.
Kang, Dae Gill,Moon, Mi Kyoung,Choi, Deok Ho,Lee, Jun Kyoung,Kwon, Tae Oh,Lee, Ho Sub Elsevier 2005 european journal of pharmacology Vol.524 No.1
<P><B>Abstract</B></P><P>Vasorelaxant and anti-inflammatory effects of a 1,2,3,4,6-penta-<I>O</I>-galloyl-β-<SMALL>D</SMALL>-glucose (PGG) isolated from the root barks of <I>Paeonia suffruticosa</I> and possible mechanisms responsible were investigated. PGG induced a concentration-dependent relaxation of the phenylephrine-precontracted rat aorta. This effect disappeared with the removal of functional endothelium. Pretreatment of the aortic tissues with either <I>N</I><SUP>G</SUP>-nitro-<SMALL>L</SMALL>-arginine methyl ester (<SMALL>L</SMALL>-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-α]-quinoxalin-1-one (ODQ) inhibited the relaxation induced by PGG. Incubation of human umbilical vein endothelial cells (HUVECs) or carotid arteries isolated from rats with PGG increased the production of cGMP in a dose-dependent manner, but this effect was blocked by pretreatment with <SMALL>L</SMALL>-NAME and ODQ, respectively. PGG treatment attenuated tumor necrosis factor-α (TNF-α)-induced nuclear factor-kappaB (NF-κB) p65 translocation in human umbilical vein endothelial cells. In addition, PGG suppressed the expression levels of adhesion molecules including intracellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) induced by TNF-α. TNF-α-induced monocyte chemoattractant protein-1 (MCP-1) expression was also attenuated by addition of PGG. PGG treatment inhibited cellular adhesion of U937 cells onto human umbilical vein endothelial cells induced by TNF-α. Taken together, the present study suggests that PGG dilates vascular smooth muscle and suppresses the vascular inflammatory process via endothelium-dependent nitric oxide (NO)/cGMP signaling.</P>
Kang, Dae Gill,Cao, Li Hua,Lee, Jun Kyoung,Choi, Deok Ho,Kim, Seung Ju,Lee, Hyuck,Kim, Jin Sook,Lee, Ho Sub Institute for Advanced Research in Asian Science a 2006 The American journal of Chinese medicine Vol.34 No.4
<P>The butanol extract of Phellinus igniarius (BPI) induced relaxation of the phenylephrin e-precontracted rat aorta in a dose-dependent manner, and its effect was abolished by the removal of functional endothelium. Pretreatment of the aortic tissues with N(G)-nitro-L-arginine methyl ester (L-NAME), methylene blue, or 1H-[1,2,4]-oxadiazole-[4,3-alpha]-quinoxalin1-one (ODQ) inhibited the vascular relaxation induced by BPI. BPI-induced vascular relaxations were also markedly attenuated by the addition of verapamil or diltiazem, while the relaxant effect of BPI was not blocked by pretreatment with indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, or propranolol. Incubation of endothelium-intact rat aorta with BPI increased the production of cGMP in a dose-dependent manner. These results suggest that BPI dilates vascular smooth muscle via endothelium-dependent nitric oxide-cGMP signaling pathway, with the possible involvement of L-type Ca(2+) channels.</P>