参元丹干预氧化三甲胺诱导人脐静脉内皮细胞损伤的机制研究

The Effect of Shenyuandan on the Injury of HUVEC Induced by Trimethylamine Oxide

目的:探讨参元丹对氧化三甲胺(TMAO)诱导人脐静脉内皮细胞(HUVEC)损伤的干预作用及机制。方法:建立TMAO诱导的HUVEC细胞损伤模型,将HUVEC分为正常对照组、模型组(300μmol/L TMAO)、参元丹低剂量组(300μmol/L TMAO+25μg/mL参元丹)、参元丹中剂量组(300μmol/L TMAO+50μg/mL参元丹)、参元丹高剂量组(300μmol/L TMAO+100μg/mL参元丹)。分别检测各组细胞中活性氧(ROS)、丙二醛(MDA)、白细胞介素(IL)-1β含量。结果:TMAO可诱导HUVEC发生氧化应激反应及炎症反应,参元丹可降低TMAO损伤细胞内ROS、MDA水平(P<0.05),同时抑制IL-1β的表达水平(P<0.05)。结论:参元丹可能通过抑制氧化应激反应及炎症反应,减轻TMAO诱导的内皮细胞损伤。

Objective:To investigate the effect of Shenyuandan on trimethylamine oxide(TMAO)induced injury of human umbilical vein endothelial cells(HUVEC).Methods:TMAO induced HUVEC cell damage model was established.HUVEC were divided into normal control group,model group(300μmol/L TMAO),Shenyuandan low-dose group(300μmol/L TMAO+25μg/mL Shenyuandan),Shenyuandan medium-dose group(300μmol/L TMAO+50μg/mL Shenyuandan),and Shenyuandan high-dose group(300μmol/L TMAO+100μg/mL Shenyuandan).The contents of reactive oxygen species(ROS),malondialdehyde(MDA),interleukin(IL)-1βin each group were detected.Results:TMAO could induce oxidative stress and inflammation in HUVEC.Shenyuandan could decrease the ROS and MDA levels in TMAO injured cells(P<0.05),and inhibit the expression level of IL-1β(P<0.05).Conclusion:endothelial cell Shenyuandan may reduce TMAO induced damage by inhibiting oxidative stress and inflammation.