通心络对氧化低密度脂蛋白损伤血管内皮细胞的保护作用  

Tongxinluo protects vascular endothelial cells against ox-LDL-induced injury

作　　者：李红蓉[1] 常成成[2] 郭勇英[3] 李辉欣 贾振华[1] 

机构地区：[1]河北医科大学研究生学院,石家庄医学硕士050017 [2]南京中医药大学基础医学院,南京210029 [3]河北省中医院呼吸科,石家庄050017 [4]河北以岭医药研究院/国家中医药管理局重点研究室,石家庄050035

出　　处：《医学研究生学报》2015年第11期1128-1132,共5页Journal of Medical Postgraduates

基　　金：国家重点基础研究发展计划973项目(2012CB518600)

摘　　要：目的氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)损伤血管内皮细胞是动脉粥样硬化的重要起始环节之一。文中旨在观察通心络对ox-LDL诱导损伤的血管内皮细胞的保护作用。方法采用ox-LDL(终浓度为30mg/L)造成血管内皮细胞氧化应激损伤模型,将人脐静脉内皮细胞(human umbilical vein endothelial cell,HUVEC)分为正常对照组、模型组、通心络高、中、低剂量组,正常对照组给予无血清DMEM培养基培养,模型组给予含ox-LDL(终浓度为30 mg/L)的无血清DMEM培养基培养24 h,通心络低、中、高剂量组给予含不同浓度通心络(终浓度为50、100、150 mg/L)预培养4 h后加入ox-LDL(终浓度为30 mg/L)继续培养24 h。MTS法检测各组细胞的生存活性;试剂盒检测各组细胞上清液中NO含量、SOD的活力和线粒体膜电位变化;Western blot法检测各组细胞诱导型NO合酶(inducible nitric oxide synthase,i NOS)、基质金属蛋白酶9(matrix metalloproteinase9,MMP9)、核因子κB(nuclear factor kappa B,NF-κB)p65蛋白表达情况。结果与正常对照组比较,模型组HUVEC生存活性明显降低[(100.00±2.23)%vs(73.89±0.67)%,P<0.01],与模型组比较,通心络中、高剂量组HUVECs生存活性[(92.15±0.76)%、(97.19±1.45)%]明显提高(P<0.01)。与正常对照组细胞线粒体膜电位、细胞培养液中NO含量、SOD活力比较,模型组明显降低(P<0.01);而通心络低、中、高剂量组较模型组明显升高(P<0.01)。与正常对照组i NOS、MMP9、NF-κBp65蛋白表达比较,模型组明显升高(P<0.01);而通心络低、中,高剂量组较模型组明显降低(P<0.05)。结论通心络有较强的抗氧化、抗炎能力,可减轻ox-LDL对血管内皮细胞的损伤。Objective Oxidized low-density lipoprotein（ ox-LDL） induces vascular endothelial cell injury,which is one of the factors initiating atherosclerosis. This study aimed to investigate the protective effect of Tongxinluo（ TXL） on vascular endothelial cells with ox-LDL-induced injury. Methods Human umbilical vein endothelial cells（ HUVEC） were cultured in vitro and divided into five groups： normal control,oxidative stress injury（ OSI） model,and high,medium and low dose TXL. The HUVECs were incubated with ox-LDL at the concentration of 30 mg / L for 24 hours to induce oxidative stress injury and then treated with TXL at 50,100 and150 mg / L for 4 hours,followed by 24 hour incubation with 30 mg / L ox-LDL added to the culture medium. The viability of the cells was detected by MTS assay,the nitric oxide（ NO） content,superoxide dismutase（ SOD） activity and mitochondrial membrane potential（ MMP） in the cell culture supernatant were measured with respective kits,and the expressions of i NOS,MMP9,and NF-κBp65proteins were determined by Western blot. Results The HUVECs of the OSI model group showed a significant decrease in cell viability compared with the normal control,（ [73. 89 ± 0. 67] vs [100. 00 ± 2. 23]%,P〈0. 01） but a remarkably increase after treated with medium and high dose TXL（ [92. 15 ± 0. 76]% and [97. 19 ± 1. 45]%,P〈0. 01）. The MMP,NO content,and SOD activity were markedly reduced in the model group（ P〈0. 01） but elevated in the low,medium,and high dose TXL groups（ P〈0. 01）. The expressions of the i NOS,MMP9,and NF-κBp65 proteins were significantly up-regulated in the model group（ P〈0. 01） but down regulated in the low,medium,and high dose TXL groups（ P〈0. 05）. Conclusion TXL has the effects of anti-oxidation and anti-inflammation and can protect vascular endothelial cells against ox-LDL-induced injury.

关 键 词：通心络 血管内皮细胞 氧化低密度脂蛋白 

分 类 号：R259[医药卫生—中西医结合]