低密度脂蛋白对人肾小球系膜细胞产生炎性介质的影响  

LDL INDUCED PRODUCTION OF INFLAMMATORY MEDIATORS IN CULTURED HUMAN GLOMERULAR MESANGIAL CELLS

作　　者：王晓燕[1,2] 潘晓勤[1,2] 高远赋[1,2] 胡明昌 甘卫华[1,2] 姜新猷 

机构地区：[1]南京军区南京总医院儿科 [2]南京医科大学小儿肾脏病研究中心

出　　处：《肾脏病与透析肾移植杂志》1997年第1期31-35,共5页Chinese Journal of Nephrology,Dialysis & Transplantation

摘　　要：目的：探讨脂蛋白在肾小球损伤中的作用，观察人低密度脂蛋白（ＬＤＬ）对体外培养的人肾小球系膜细胞（ＧＭＣ）产生活性氧（ＲＯＳ）、血小板活化因子（ＰＡＦ）、肿瘤坏死因子（ＴＮＦ）和乳酸脱氢酶（ＬＤＨ）的影响，并与经ＬＤＬ刺激后ＧＭＣ的增殖水平相比较。方法：将ＧＭＣ加或不加ＬＤＬ刺激，分别收集３０ｍｉｎ、１８ｈ或４８ｈ后的上清，测定其Ｈ２Ｏ２、Ｏ－２、ＴＮＦ、ＰＡＦ和ＬＤＨ的水平，以四唑蓝（ＭＴＴ）摄入试验，测定刺激４８ｈ后细胞于波长５７０ｎｍ的吸光度。结果：经ＬＤＬ刺激３０ｍｉｎ，细胞上清中Ｈ２Ｏ２和Ｏ－２的含量均高于对照，在浓度＜１００ｍｇ／Ｌ时，增高更为明显。刺激１８ｈ，上清中ＰＡＦ的水平亦有类似变化。刺激４８ｈ时，上清中ＬＤＨ的水平较１８ｈ时有所增加，且在ＬＤＬ１００ｍｇ／Ｌ时高达对照的３倍以上；细胞的吸光度亦增加，大于２００ｍｇ／Ｌ时则低于对照。ＬＤＬ刺激１８和４８ｈ的细胞上清对ＴＮＦ敏感株的杀伤率虽有增加，但均未达５０％。结论：ＬＤＬ可增加体外培养的人ＧＭＣ上清中活性氧、ＰＡＦ和ＬＤＨ，或ＴＮＦ等水平，因而可通过多种途径介导肾小球损伤，包括刺激ＧＭＣ产生或释放炎性介质和影响系膜细胞增殖。OBJECTIVE To study the effects of LDL on the production of inflammatory mediators in glomerular mesangial cells and to look at the mechanism of LDL induced glomerular injury. METHODOLOGY Human mesangial cells (GMC) were treated with or without human LDL. The effects on cell proliferation were compared between LDL stimulated GMC and the control. Levels of H 2O 2 and O 2, PAF, TNF and LDH in supernatant were determined and compared. RESULTS We found that the levels of H 2O 2and O - 2in supernatant were markedly increased by LDL stimulating for 30 minutes at concentrations of 10～100 mg/L. The levels didn't continue to increase as LDL concentration exceeds 100 mg/L. The curves of ROS, PAF, LDH production were similar to that of cell proliferation. The L 929 cell mortality of the supernatants were higher than controls. CONCLUSION LDL can increase ROS, PAF, LDH, and perhaps TNF productions in human GMC in vitro in a dose dependent manner below 100 mg/L. Our findings suggest that LDL might mediate glomerular injury through stimulating the production of mediators as well as affecting the proliferation of GMC.

关 键 词：低密度脂蛋白 系膜细胞 炎性介质 肾小球疾病 

分 类 号：R692.602[医药卫生—泌尿科学]