Induction of inducible nitric oxide synthase by ginsenosides in cultured porcine endothelial cells

Mechanism of Nitric oxide (NO) production by ginsenosides was investigated in cultured porcine endothelial cells. β-Nicotinamide adenine dinucleotide phosphate (β-NADPH) staining showed that the NO production was significantly enhanced by the presence of 40 μg/ml ginsenosides with 10 μM L-arginine a...

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Veröffentlicht in:Life sciences (1973) 2000-11, Vol.67 (24), p.2983-2989
Hauptverfasser: Li, Zhiyuan, Niwa, Yasuharu, Sakamoto, Sadaichi, Shono, Masayuki, Chen, Xiu, Nakaya, Yutaka
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container_end_page 2989
container_issue 24
container_start_page 2983
container_title Life sciences (1973)
container_volume 67
creator Li, Zhiyuan
Niwa, Yasuharu
Sakamoto, Sadaichi
Shono, Masayuki
Chen, Xiu
Nakaya, Yutaka
description Mechanism of Nitric oxide (NO) production by ginsenosides was investigated in cultured porcine endothelial cells. β-Nicotinamide adenine dinucleotide phosphate (β-NADPH) staining showed that the NO production was significantly enhanced by the presence of 40 μg/ml ginsenosides with 10 μM L-arginine after 12 h incubation. NO production was suppressed by addition of 0.5 μM N ω-Nitro-L-arginine (L-NNA), an inhibitor of NO synthases (NOSs), to the incubation medium. In addition, the immunoreactive signals of inducible NOS (iNOS) were appeared in endothelial cells after 12-h incubation of ginsenosides, whereas the signals were not observed in non-treated cells. Our findings suggest that ginsenosides can enhance NO production by induction of iNOS in addition to its direct effect on endothelial cells by increasing intracellular Ca 2+ concentration.
doi_str_mv 10.1016/S0024-3205(00)00880-8
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NO production was suppressed by addition of 0.5 μM N ω-Nitro-L-arginine (L-NNA), an inhibitor of NO synthases (NOSs), to the incubation medium. In addition, the immunoreactive signals of inducible NOS (iNOS) were appeared in endothelial cells after 12-h incubation of ginsenosides, whereas the signals were not observed in non-treated cells. 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NO production was suppressed by addition of 0.5 μM N ω-Nitro-L-arginine (L-NNA), an inhibitor of NO synthases (NOSs), to the incubation medium. In addition, the immunoreactive signals of inducible NOS (iNOS) were appeared in endothelial cells after 12-h incubation of ginsenosides, whereas the signals were not observed in non-treated cells. 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NO production was suppressed by addition of 0.5 μM N ω-Nitro-L-arginine (L-NNA), an inhibitor of NO synthases (NOSs), to the incubation medium. In addition, the immunoreactive signals of inducible NOS (iNOS) were appeared in endothelial cells after 12-h incubation of ginsenosides, whereas the signals were not observed in non-treated cells. Our findings suggest that ginsenosides can enhance NO production by induction of iNOS in addition to its direct effect on endothelial cells by increasing intracellular Ca 2+ concentration.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>11133010</pmid><doi>10.1016/S0024-3205(00)00880-8</doi><tpages>7</tpages></addata></record>
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source MEDLINE; Elsevier ScienceDirect Journals
subjects Animals
Aorta
Arginine - pharmacology
Ca 2+ influx
Calcium - metabolism
Cells, Cultured
Drug Combinations
Endothelial cell
Endothelium, Vascular - cytology
Endothelium, Vascular - drug effects
Endothelium, Vascular - enzymology
Enzyme Induction
Enzyme Inhibitors - pharmacology
Ginsenosides
Immunohistochemistry
Nitric oxide production
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - biosynthesis
Nitric Oxide Synthase Type II
omega-N-Methylarginine - pharmacology
Saponins - pharmacology
Swine
title Induction of inducible nitric oxide synthase by ginsenosides in cultured porcine endothelial cells
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