人参皂甙抑制肿瘤坏死因子α介导的内皮细胞炎症反应

Ginsenoside Rb1 Inhibits Tumor Necrosis Factor-α Induced Inflammation of Human Umbilical Vein Endothelial Cell

目的探讨人参皂甙Rb1能否抑制人脐静脉内皮细胞中肿瘤坏死因子α引起的细胞炎症反应的发生。方法将细胞分成四组:对照组(不经任何药物处理)、肿瘤坏死因子α组、人参皂甙Rb1组和肿瘤坏死因子α加人参皂甙Rb1组,分别培养16 h。提取各组细胞mRNA,用实时荧光定量PCR和流式细胞仪测定血管细胞黏附分子1的表达水平;用标记上Calce in-AM的人单核细胞检测人脐静脉内皮细胞单分子层的黏附性;用超氧化物阴离子荧光探针DHE在流式细胞仪上测定超氧阴离子产物,并用荧光探针JC-1检测线粒体膜电位变化。结果人参皂甙Rb1预处理能有效阻止肿瘤坏死因子α诱导的血管细胞黏附分子1 mRNA增高,并减弱由其导致的单核细胞对人脐静脉内皮细胞的黏附性增加。人参皂甙Rb1还能减少肿瘤坏死因子α诱导的超氧阴离子产物增加,并抑制由其引起的线粒体膜电位衰减。结论人参皂甙Rb1对炎症及心血管疾病有潜在的治疗作用。

Aim To investigate whether Rbl could block tumor necrosis factor-α （TNF-ct）induced inflammation in human umbilical vein endothelial cell （ HUVEC ）. Methods HUVEC were treated with TNF-α （0.5 μg/L） and/ or Rbl （ 15 mg/L） for 16 hours. The mRNA level of vascular cell adhesion molecule-1 （ VCAM-1 ） was determined by real-time PCR and flow cytometry, respectively. Human macrophage THP-1 labeled with a fluorescent dye （Calcein-AM） was used for the adhesion assay on HUVEC monolayer. Dihydroethidium （DHE ） was used to demonstrate in situ levels of superoxide production. JC-1 dye was used to measure changes in mitochondrial membrane potential. Results TNF-α treatment significantly increased the mRNA expression of VCAM-1 in HUVEC, as compared to controls. Rbl pretreatment blocked the TNF-α induced mRNA expression of VCAM-1, and also effectively blocked THP-1 adhesions. Furthermore, Rbl reduces TNF-α induced increase of superoxide anion production and inhibits TNF-α induced decrease of mitochondrial membrane potential in HUVEC. Conclusion These data suggested that Rbl might have potential therapeutic effects in controlling inflammation in vascular diseases.