摘要
目的:研究乌司他丁对炎症因子诱导的体外培养的大鼠肺微血管内皮细胞通透性和细胞因子产生的影响。方法:体外培养大鼠肺微血管内皮细胞分组进行实验:①对照组:内皮细胞培养液中加入生理盐水或乌司他丁;②炎症因子刺激组:因培养液中分别含烫伤血清、胰蛋白酶、前列腺素E_2(PGE_2)、缓激肽、组胺而分为5个炎症因子刺激亚组;③乌司他丁处理组:培养液中在含上述各炎症刺激因子基础上分别加入乌司他丁而分成5个乌司他丁处理组。采用Transwell方法测定各组单层内皮细胞对牛血清白蛋白(BSA)通透性的变化;取各组细胞培养上清液,用酶联免疫吸附方法(ELISA)检测肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的水平。结果:各炎症因子刺激组肺微血管内皮细胞通透系数均比对照组显著增高,TNF-α和IL-6的产生量也显著增多(P均<0.01);乌司他丁处理组中烫伤血清和胰蛋白酶组的血管内皮细胞通透系数及TNF-α和IL-6产生量比相应炎症因子刺激组显著降低(P均<0.01),但组胺、缓激肽和PGE_2刺激后乌司他丁处理组与相应炎症因子刺激组比较,上述指标无显著改变(P均>0.05)。结论:乌司他丁能显著抑制烫伤血清和胰蛋白酶引起的肺微血管内皮细胞通透性及TNF-α和IL-6水平增高,对组胺、缓激肽和PGE_2引起的肺微血管内皮细胞通透性增加和促炎细胞因子产生无显著影响。
Objective： To investigate the effects of ulinastatin on changes in microvascular endothelial permeability and cytokine production induced by inflammatory factor. Methods：The cultured pulmonary microvascular endothelial cells （PMECs） were divided into 3 groups：①Control group： Normal saline or ulinastatin was added into cell culture. ② Inflammatory factors-stimulating group： It was redivided into five subgroups in which scald serum, trypsin, bradykinin, histamine or prostaglandin F4 （PGE2）was added respectively into PMECs culture. ③ Ulinastatin treatment group： It was redivided into five subgroups in which ulinastatin was added separately into PMECs culture in which inflammatory factors were respectively added as inflammatory factors-stimulating group. The permeability of monolayer PMECs was determined by the method of Transwell. The production of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） was determined by enzyme-linked immunoadsorbent assay （ELISA）. Results：The permeability of monolayer PMECs, and the production of TNF-a and IL-6 in each inflammatory factor-stimulating group were significantly increased compared with those of control group （P〈0. 01）. The permeability of PMECs, and the production of pro-inflammatory factors in scald serum and trypsin groups were markedly lowered after ulinastatin treatment compared with those groups without ulinastatin treatment （all P 〈0. 01）, while the levels of bradykinin, histamine and PGF4 groups were not lowered compared with non-ulinastatin treatment groups（P〈0. 05）. Conclusions：The results indicate that ulinastatin significantly inhibit the increase in the permeability of PMECs and the production of TNF-α and IL-6 induced by the scald serum and trypsin,while it has no significant effect on the increased permeability of PMECs and pro-inflammatory factors released from PMECs after treatment with bradykinin, histamine and PGF4.
出处
《感染．炎症．修复》
2011年第4期224-227,共4页
Infection Inflammation Repair
基金
天普研究基金资助课题(02100917)
关键词
乌司他丁
血管内皮细胞
肺
内皮细胞通透性
炎症因子
Ulinastatin Pulmonary vascular endothelium Vasopermeability Inflammatory factor
