肖振宇, 张俊平, 陆峰, 张大志, 郑钦岳. 商陆皂苷甲对细胞间粘附的影响商陆皂苷甲对细胞间粘附的影响J. 药学学报, 2003, 38(10): 728-730.
引用本文: 肖振宇, 张俊平, 陆峰, 张大志, 郑钦岳. 商陆皂苷甲对细胞间粘附的影响商陆皂苷甲对细胞间粘附的影响J. 药学学报, 2003, 38(10): 728-730.
XIAO Zhen-yu, ZHANG Jun-ping, LU Feng, ZHANG Da-zhi, ZHENG Qin-yue. Effect of esculentoside A on cellular adhesionJ. Acta Pharmaceutica Sinica, 2003, 38(10): 728-730.
Citation: XIAO Zhen-yu, ZHANG Jun-ping, LU Feng, ZHANG Da-zhi, ZHENG Qin-yue. Effect of esculentoside A on cellular adhesionJ. Acta Pharmaceutica Sinica, 2003, 38(10): 728-730.

商陆皂苷甲对细胞间粘附的影响商陆皂苷甲对细胞间粘附的影响

Effect of esculentoside A on cellular adhesion

  • 摘要: 目的研究商陆皂苷甲(EsA)对细胞间粘附的影响,并观察粘附分子ICAM-1和CD18 mRNA的表达水平。方法用血细胞计数仪计数的方法考察在脂多糖(LPS)诱导下,EsA对中性粒细胞与内皮细胞间粘附的影响。用逆转录聚合酶链反应(RT-PCR)的方法测定内皮细胞ICAM-1 mRNA和中性粒细胞CD18 mRNA的表达水平。结果EsA在3~12×10-6 μmol·L-1能降低LPS作用下中性粒细胞与内皮细胞间高水平的粘附率,且能降低LPS诱导下内皮细胞ICAM-1 mRNA和中性粒细胞CD18 mRNA的表达。结论EsA能抑制LPS作用下中性粒细胞与内皮细胞间的粘附可能是其抗炎机制之一,降低粘附分子的表达可能是其影响细胞间粘附的重要作用机制。

     

    Abstract: AimTo investigate the anti-inflammatory mechanism of esculentoside A (EsA) and to observe the effects of EsA on cellular adhesion between human umbilical vein endothelial cell (VEC304) and human neutrophil and to further observe the mRNA expression of intercellular adhesion molecule-1(ICAM-1) and cluster of differentiation 18(CD18). MethodsThe hemocyte counting method was used for assaying the adhesion rate between VEC304 and neutrophil. The RT-PCR method was used for measuring the mRNA expression of ICAM-1 and CD18.ResultsThe adhesion rate between VEC304 and neutrophil was increased with treatment of lipopolysaccharide(LPS). EsA (3-12×10-6 μmol·L-1) was shown to inhibit the high cellular adhesion induced by LPS. A further investigation of adhesion molecules mRNA expression was undertaken using semi-quantitative reverse transcribed polymerase chain reaction (RT-PCR).The results of RT-PCR from VEC304 and human neutrophil treating with LPS showed that ICAM-1 and CD18 mRNA expressions were higher than those of normal cells, while this increased expression of ICAM-1 and CD18 mRNA was remarkably attenuated by the addition of EsA.ConclusionEsA was found to inhibit the increased adhesion rate induced by LPS.Moreover, LPS induced high expression of ICAM-1 and CD18 was inhibited with treatment of EsA.It might be involved in the mechanisms of anti-inflammation of EsA.

     

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