人参皂苷Re对肿瘤坏死因子-α诱导的白细胞活化的抑制作用及机制

Effect and Mechanism of Ginsenoside Re on TNF-α-induced Leukocyte Activation

目的研究人参皂苷Re对肿瘤坏死因子-α诱导的白细胞活化的作用及其机制。方法提取并培养人外周血中性白细胞,用酶标仪和流式细胞仪体外观察肿瘤坏死因子-α(20 ng/ml)对中性白细胞黏附相关指标MPO的分泌以及白细胞表面黏附分子CD11b和CD18的表达的诱导作用,同时观察肿瘤坏死因子-α(20 ng/ml)对中性白细胞跨内皮细胞迁移的诱导作用,并测定不同浓度人参皂苷Re对以上变化的影响。结果人参皂苷Re可以剂量依赖性地明显抑制肿瘤坏死因子-α诱导的黏附于内皮细胞表面白细胞MPO的分泌和黏附分子CD11b、CD18的表达,明显抑制肿瘤坏死因子-α诱导的中性白细胞跨内皮细胞的迁移。结论人参皂苷Re可以抑制由肿瘤坏死因子-α诱导的白细胞的活化,包括白细胞与内皮细胞的黏附和游出,该作用与抑制白细胞表面黏附分子CD11b和CD18的表达相关。

Objective To explore the effect and mechanism of ginsenoside Re on tumor necrosis factor-α（TNF-α）-induced leukocyte activation.Methods Leukocytes were separated from human whole blood and cultured in RPMI medium.The stimulation effect of TNF-α（20 ng/ml） on leukocyte adhesion related parameters,such as the activity of myeloperoxidase（MPO） release and the expression of leukocyte adhesion molecules CD11b and CD18,was assayed by the microreader and flow cytometry,respectively.In addition,leukocyte migration across the endothelium evoked by TNF-α（20 ng/ml） was assessed.Furthermore,the effect of different concentrations of ginsenoside Re on above-mentioned parameters were evaluated at the same time.Results Ginsenoside Re can dose-dependently inhibit TNF-α-induced leukocyte adhesion to endothelial cells,including MPO release and expression of leukocyte adhesion molecules CD11b and CD18 as well as leukocyte transmigration across the endothelium.Conclusion Ginsenoside Re can inhibit TNF-α induced activation of leukocytes,including leukocyte adhesion to endothelial cells and transmigration.This role is related to the inhibition of the expression of leukocyte adhesion molecules CD11b and CD18.