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Chuncheon, South Korea

Han Wha Pharma Co. | Date: 2004-06-18

Nutritional and dietary supplements.

A method for preventing and treating thrombotic disorders in a subject in need thereof comprising, administering a pharmaceutical composition comprising an extract of

Lee J.-O.,University of Strasbourg | Lee J.-O.,Hanwha Pharma. Co. | Auger C.,University of Strasbourg | Kang M.,Hanwha Pharma. Co. | And 3 more authors.

Lindera obtusiloba is a medicinal herb traditionally used in Asia for improvement of blood circulation, treatment of inflammation, and prevention of liver damage. A previous study has shown that an ethanolic extract of Lindera obtusiloba stems (LOE) has vasoprotective and antihypertensive effects. The possibility that Lindera obtusiloba improves endothelial function and metabolic parameters in type 2 diabetes mellitus (T2DM) remains to be examined. Therefore, the aim of the present study was to determine the potential of LOE to prevent the development of an endothelial dysfunction, and improve metabolic parameters including hyperglycemia, albuminuria and physical exercise capacity in db/db mice, an experimental model of T2DM. The effect of LOE (100 mg/kg/day by gavage for 8 weeks) on these parameters was compared to that of an oral antidiabetic drug, pioglitazone (30 mg/kg/day by gavage). Reduced blood glucose level, body weight and albumin-creatinine ratio were observed in the group receiving LOE compared to the control db/db group. The LOE treatment improved endothelium-dependent relaxations, abolished endothelium-dependent contractions to acetylcholine in the aorta, and normalized the increased vascular oxidative stress and expression of NADPH oxidase, cyclooxygenases, angiotensin II, angiotensin type 1 receptors and peroxynitrite and the decreased expression of endothelial NO synthase in db/db mice. The angiotensin-converting enzyme (ACE) activity was reduced in the LOE group compared to that in the control db/db group. LOE also inhibited the activity of purified ACE, COX-1 and COX-2 in a dose-dependent manner. In addition, LOE improved physical exercise capacity. Thus, the present findings indicate that LOE has a beneficial effect on the vascular system in db/db mice by improving endothelium-dependent relaxations and vascular oxidative stress most likely by normalizing the angiotensin system, and also on metabolic parameters, and these effects are associated with an enhanced physical exercise capacity. © 2013 Lee et al. Source

Lee J.-O.,Hanwha Pharma. Co. | Chang K.,Catholic University of Korea | Kim C.Y.,Korea Institute of Science and Technology | Jung S.H.,Korea Institute of Science and Technology | Oak M.-H.,Hanwha Pharma. Co.
Journal of Cardiovascular Pharmacology

Lysimachia clethroides is widely used in traditional herbal medicine for many purposes, especially for blood vessel-related diseases in Korea and East Asia. Experiments were undertaken to determine whether hydro-alcoholic extract obtained from L. clethroides (LCE) has vasorelaxant activity in the rat aorta rings and, if so, to elucidate the underlying mechanism. Rat aorta rings were suspended in organ chambers for the measurement of changes in isometric tension in the presence or absence of several inhibitors. LCE induced endothelium-dependent vasodilation (ED50 = 6.1 μg/mL) and that was abolished by nitric oxide synthase inhibitor, N-nitro-L-arginine, and guanylyl cyclase inhibitor, 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one, PI3-kinase inhibitor, wortmannin, and cell permeable superoxide dismutase. In addition, LCE decreased vessels contraction by phenylephrine. Prostaglandin synthesis inhibitor, indometacin, and inhibitors of endothelium-derived hyperpolarizing factor, charybdotoxin plus apamin, did not affect vasodilatory effect of LCE. In cultured endothelial cells, LCE-induced phosphorylation of serine 1177-endothelial nitric oxide synthase and serine 473-Akt. LCE inhibited strongly nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity in smooth muscle cells and angiotensin II-induced contraction of rat aorta. Finally, increased oxidative stress in rat aorta-induced by angiotensin II is ameliorated by LCE. Taken together, LCE induces an endothelium-dependent vasodilation and might be involved, at least in part, the activation of the nitric oxide-cyclic guanosine monophosphate pathway. In addition, LCE decreases oxidative stress in aorta by inhibition of NADPH oxidase activity. The present findings indicate that LCE could be a candidate of herbal medicine for cardiovascular diseases associated with disturbed NO production and endothelial dysfunction. Copyright © 2010 by Lippincott Williams & Wilkins. Source

Lee J.-O.,Hanwha Pharma. Co. | Kim C.,Korea Institute of Science and Technology | Oak M.-H.,Hanwha Pharma. Co.
Biomolecules and Therapeutics

Several studies have shown that plant-derived polyphenols reduce cardiovascular accidents in high-risk patients and the inhibition of platelet function may be responsible for part of this benefit. Lindera obtusiloba is widely used in traditional herbal medicine for the treatment of cardiovascular and inflammatory diseases. Therefore, the antiplatelet and antithrombotic activities of Lindera obtusiloba Extracts (LOE) on in vitro platelet aggregation, radical scavenging activity and in vivo murine pulmonary thrombosis were examined. LOE was able to directly scavenge the stable DPPH radical in a concentration-dependent manner and its IC50 value was 3.9 ± 0.1 μg/ml. LOE significantly inhibited collagen- and ADP-induced platelet aggregation in a concentration-dependent manner and its IC50 value is 0.9 ± 0.1 mg/ml and 0.4 ± 0.1 mg/ml respectively. The inhibitory effect of LOE was comparable to aspirin (IC50 values were 1.0 ± 0.5 and 1.0 ± 0.7 mg/ml, respectively). Furthermore, oral administration of LOE suppressed the death of mice with pulmonary thrombosis induced by intravenous injection of collagen plus epinephrine. Taken together, our results suggest LOE may be a promising candidate for antithrombotic agent, and the antithrombotic effect of LOE may be due to, at least in part, antiplatelet activity. Source

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