原花青素B2对过氧化氢诱导人脐静脉内皮细胞株EA.hy926氧化损伤的影响研究  

Influence of procyanidine B2 on oxidative damage of human umbilical vein endothelial cell line induced by hydrogen peroxide

作　　者：沈建中[1] 姚远 刘大伟 Shen Jianzhong;Yao Yuan;Liu Dawei(Department of Cardiovascular Medicine,Peking Union Medical College Hospital,Beijing 100086,China)

机构地区：[1]北京市北京协和医院心血管内科,北京100086 [2]北京中医医院平谷医院心血管科,北京101200

出　　处：《中国循证心血管医学杂志》2019年第11期1358-1361,1365,共5页Chinese Journal of Evidence-Based Cardiovascular Medicine

基　　金：中国医学科学院医学与健康科技创新工程(2016-12M-1-011)

摘　　要：目的探究原花青素B2(PB2)对过氧化氢(H2O2)诱导的人脐静脉内皮细胞株EA.hy926氧化损伤的影响及其可能机制。方法体外培养人脐静脉内皮细胞株EA.hy926,将细胞随机分为5组,即对照组、H2O2组、α-生育酚组(30μMα-tocopherol)、2μM PB2组及10μM PB2组,分别给予不同处理。对照组仅加入细胞培养液处理;H2O2组在对照组基础上加用H2O2,终浓度为200μmol/L;α-生育酚处理组在对照组基础上加用H2O2及α-生育酚(α-tocopherol),终浓度分别为200μmol/L及30μmol/L;2μM PB2组在对照组基础上加用H2O2及PB2,终浓度分别为200μmol/L及2μmol/L;10μM PB2组在对照组基础上加用H2O2及PB2,终浓度分别为200μmol/L及10μmol/L。对各组进行人类EA.hy926内皮细胞的生长分析及PB2对H2O2诱发人类EA.hy926内皮细胞DNA损伤、脂质过氧化和活性氧(ROS)的影响检测。结果与对照组比较,H2O2处理组的细胞数目明显降低,差异有统计学意义(P<0.05);与H2O2组相比,α-生育酚处理组、2μmol/L和10μmol/L PB2处理组的细胞数目均明显增加,差异均有统计学意义(P均<0.05)。与对照组比较,H2O2处理组细胞DNA损伤显著,差异有统计学意义(P<0.05);与H2O2处理组对比,2μmol/L PB2处理组、10μmol/L PB2处理组、α-生育酚处理组对H2O2所诱发的DNA损伤明显抑制,差异有统计学意义(P<0.05),抑制率分别为24%、55%和95%。与对照组比较,H2O2处理组的丙二醛(MDA)、ROS水平显著上升,差异有统计学意义(P<0.05)。与H2O2处理组对比,2μmol/L PB2处理组、10μmol/L PB2处理组和α-生育酚处理组明显抑制H2O2诱发人类EA.hy926内皮细胞MDA、ROS的产生,差异均有统计学意义(P<0.05),抑制率分别为21%、42%、49%和18%、41%、80%。结论PB2能够显著抑制H2O2诱发的人类EA.hy926内皮细胞ROS的生成,降低氧化损伤从而达到保护内皮细胞的效果。Objective To study the influence of procyanidine B2(PB2)on oxidative damage of human umbilical vein endothelial cell line(EA.hy926)induced by hydrogen peroxide(H2O2)and possible mechanism.Methods EA.hy926 were cultured in vitro,and divided randomLy into 5 groups:control group,H2O2 group,α-tocopherol group(30μM),PB2 group 1(2μM)and PB2 group 2(10μM).The control group was treated with DMEM,H2O2 group was treated with DMEM and H2O2(final concentration=200μmol/L),α-tocopherol group was treated with DMEM,H2O2(final concentration=200μmol/L)andα-tocopherol((final concentration=30μmol/L),PB2 group 1 was treated with DMEM,H2O2(final concentration=200μmol/L)and PB2(final concentration=2μmol/L),and PB2 group 2 was treated with DMEM,H2O2(final concentration=200μmol/L)and PB2(final concentration=10μmol/L).The growth of EA.hy926 was analyzed,and influence of PB2 on DNA injury,lipid peroxiation and reactive oxygen species(ROS)of EA.hy926 induced by H2O2 was detected.Results Compared with control group,the number of EA.hy926 decreased significantly in H2O2 group(P<0.05).Compared with H2O2 group,the number of EA.hy926 increased significantly inα-tocopherol group,PB2 group 1 and PB2 group 2(all P<0.05).Compared with control group,DNA injury of EA.hy926 was more significant in H2O2 group(P<0.05).Compared with H2O2 group,DNA injury of EA.hy926 was significantly inhibited in PB2 group 1,PB2 group 2 andα-tocopherol group(P<0.05),and inhibition rate was,respectively,24%,55% and 95%.Compared with control group,the levels of malondialdehyde(MDA)and ROS increased significantly in H2O2 group(P<0.05).Compared with H2O2 group,the productions of MDA and ROS in EA.hy926 induced by H2O2 were significantly inhibited in PB2 group 1,PB2 group 2 andα-tocopherol group(P<0.05),and the inhibition rate was,respectively,21%,42% and 49%,and 18%,41%and 80%.Conclusion PB2 can significantly inhibit the production of ROS in EA.hy926 induced by H2O2,relieve oxidative damage and protect endothelial cells.

关 键 词：原花青素B2 过氧化氢 人类内皮细胞氧化损伤 活性氧 

分 类 号：R543[医药卫生—心血管疾病]