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        Ginsenoside Rb1 attenuates intestinal ischemia-reperfusioninduced liver injury by inhibiting NF-κB activation

        Jin Wang,Lifen Qiao,Yongsheng Li,Guangtian Yang 생화학분자생물학회 2008 Experimental and molecular medicine Vol.40 No.6

        Intestinal ischemia-reperfusion (I/R) is an important event in the pathogenesis of multiple organ dysfunction syndrome (MODS). The aim of this study is to determine the effects of ginsenoside Rb1 on liver injury induced by intestinal I/R in rats. Adult male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group (sham group); (2) an intestinal I/R group subjected to 1 h intestinal ischemia and 2 h reperfusion (I/R group); (3) a group treated with 20 mg/kg ginsenoside Rb1 before reperfusion (Rb1-20 group); and (4) a group treated with 40 mg/kg ginsenoside Rb1 before reperfusion (Rb1-40 group). Liver and intestinal histology was observed. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) level in serum and malondialdehyde (MDA) level in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-α, MDA level and immunohistochemical expression of NF-κB and intracellular adhesion molecale- 1 (ICAM-1) in liver tissues was assayed. In addition, a western blot analysis of liver NF-κB expression was performed. Results indicated intestinal I/R induced intestinal and liver injury, which was characterized by increase of AST and ALT in serum, MDA level in intestine, MPO, TNF-α and MDA level and ICAM-1 and NF-κB expression in the liver tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated liver injury, decreased MPO, TNF-α and MDA level, NF-κB and ICAM-1 expression in liver tissues. In conclusion, ginsenoside Rb1 ablated liver injury induced by intestinal I/R by inhibiting NF-κB activation. Intestinal ischemia-reperfusion (I/R) is an important event in the pathogenesis of multiple organ dysfunction syndrome (MODS). The aim of this study is to determine the effects of ginsenoside Rb1 on liver injury induced by intestinal I/R in rats. Adult male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group (sham group); (2) an intestinal I/R group subjected to 1 h intestinal ischemia and 2 h reperfusion (I/R group); (3) a group treated with 20 mg/kg ginsenoside Rb1 before reperfusion (Rb1-20 group); and (4) a group treated with 40 mg/kg ginsenoside Rb1 before reperfusion (Rb1-40 group). Liver and intestinal histology was observed. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) level in serum and malondialdehyde (MDA) level in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-α, MDA level and immunohistochemical expression of NF-κB and intracellular adhesion molecale- 1 (ICAM-1) in liver tissues was assayed. In addition, a western blot analysis of liver NF-κB expression was performed. Results indicated intestinal I/R induced intestinal and liver injury, which was characterized by increase of AST and ALT in serum, MDA level in intestine, MPO, TNF-α and MDA level and ICAM-1 and NF-κB expression in the liver tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated liver injury, decreased MPO, TNF-α and MDA level, NF-κB and ICAM-1 expression in liver tissues. In conclusion, ginsenoside Rb1 ablated liver injury induced by intestinal I/R by inhibiting NF-κB activation.

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        Synthesis and Biological Evaluation of 3-(1H-indol-3-yl)pyrazole- 5-carboxylic Acid Derivatives

        Datong Zhang,Guangtian Wang,Chubing Tan,Weiren Xu,Yuan Pei,Lingyan Huo 대한약학회 2011 Archives of Pharmacal Research Vol.34 No.3

        A series of novel compounds bearing a 3-(1H-indol-3-yl)pyrazole-5-carboxylic acid nucleus were synthesized. Analytical and spectral data confirmed the structures of the new compounds. The structures of the regioisomers in this series were determined by 1H-NMR spectra. The title compounds were evaluated for their endothelin-1 antagonist activities. In the in vitro functional assay, compounds 23, 24, 28 and 29 exhibited significant efficacy at the concentration of 1 μg/mL, and compounds 5b, 5c, 26 and 28 were as potent as the positive control bosentan at high concentration. In the experiment to assess prevention of endothelin-1-induced sudden death in mice, compound 5b showed comparable activity to bosentan, and 30 was more potent than bosentan. The final compounds were also screened for antibacterial activity against four Gram-positive and -negative bacteria. Some of the tested compounds showed weak antibacterial activity.

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