Regulatory mechanisms of ginsenoside Rb1 on inflammatory substances in U-937 cells

碩士 === 臺北醫學大學 === 保健營養學系 === 97 === This study investigated the effects of ginsenoside Rb1 (98.8% purity) on cell regulation of inflammatory responses in human monocytes/macrophages-like U-937 cells after lipopolysacchrides (LPS) stimulation. The U-937 cells were cultured in RPMI 1640 medium supplem...

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Bibliographic Details
Main Authors: Yi-Ten, Tseng, 曾依田
Other Authors: 謝明哲
Format: Others
Language:zh-TW
Published: 2009
Online Access:http://ndltd.ncl.edu.tw/handle/75633905806601183386
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Summary:碩士 === 臺北醫學大學 === 保健營養學系 === 97 === This study investigated the effects of ginsenoside Rb1 (98.8% purity) on cell regulation of inflammatory responses in human monocytes/macrophages-like U-937 cells after lipopolysacchrides (LPS) stimulation. The U-937 cells were cultured in RPMI 1640 medium supplemented with 10% fetal calf serum. The cells were incubated at 37℃and 5% CO2 atmosphere. The U-937 cells were treated with phorbol 12-myristate 13-acetate (PMA) for differentiation into macrophages. Subsequently, the medium was replaced by fresh medium containing 0.1% bovine serum albumin and added different concentrations of ginsenoside Rb1 (5, 10, 25, 50, 100 g/ml). After 1-hour incubation, LPS was added to induce the inflammatory response. After 1 hour, cells were collected for NF-kB assays. After 23- hour incubation, the medium was collected for TNF-α, soluble intercellular adhesion molecule-1 (sICAM-1) assays and cells were collected for the determination of COX-2 protein expression. The results showed that ginsenoside Rb1 at 10-100 g/ml inhibited LPS-induced TNF-a (p < 0.05) and suppressed sICAM-1 scretion and COX-2 expression at 5-100 g/ml and 5-100 g/ml, respectively (p < 0.05). The expression of NF-kB p65 subunit was also increased when treated with ginsenoside Rb1 (50 and 100 mg/ml), and ginsenoside Rb1 at the dose of 100 mg/ml increased IkBa levels. Therefore, ginsenoside Rb1 might inhibit pro-inflammatory substances through suppressing the activation of NF-kB pathway in U-937 cells.