CAJ | 학술논문

目的:研究维持性血液透析(MHD)患者血清对体外培养人脐静脉血管内皮细胞细胞间黏附分子(ICAM-1)表达的影响及其致内皮细胞功能紊乱的机制.方法:用10%胎牛血清1640培养液(对照组,A组)、10%正常人血清1640培养液(正常人组,B组)、10% MHD患者血清1640培养液(MHD患者组,C组)分别培养人脐静脉血管内皮细胞1、3、6、12 h,用免疫组织化学方法检测ICAM-1的表达情况.结果:不同血清刺激组人脐静脉血管内皮细胞 ICAM-1表达的差异有统计学意义(P < 0.05),与A组和B组比较,C组ICAM-1表达明显增加.不同刺激时间ICAM-1表达的差别有统计学意义(P < 0.05),不同血清刺激组ICAM-1的表达与刺激时间之间存在交互效应(P < 0.05).结论:慢性肾功能衰竭MHD患者血清可促进体外培养人脐静脉血管内皮细胞 ICAM-1的表达,从而导致内皮细胞功能失调.
목적:연구유지성혈액투석(MHD)환자혈청대체외배양인제정맥혈관내피세포세포간점부분자(ICAM-1)표체적영향급기치내피세포공능문란적궤제.방법:용10%태우혈청1640배양액(대조조,A조)、10%정상인혈청1640배양액(정상인조,B조)、10% MHD환자혈청1640배양액(MHD환자조,C조)분별배양인제정맥혈관내피세포1、3、6、12 h,용면역조직화학방법검측ICAM-1적표체정황.결과:불동혈청자격조인제정맥혈관내피세포 ICAM-1표체적차이유통계학의의(P < 0.05),여A조화B조비교,C조ICAM-1표체명현증가.불동자격시간ICAM-1표체적차별유통계학의의(P < 0.05),불동혈청자격조ICAM-1적표체여자격시간지간존재교호효응(P < 0.05).결론:만성신공능쇠갈MHD환자혈청가촉진체외배양인제정맥혈관내피세포 ICAM-1적표체,종이도치내피세포공능실조.
Objective: To study the effect of serum from maintenance hemodialysis(MHD) patients on the expression of intercellular adhesion molecule-1(ICAM-1) in human umbilical vein endothelial cells(HUVEC) cultured in vitro, and the mechanism of endothelial cells dysfunction caused by serum from MHD patients thereof. Methods: HUVEC were incubated for 1 h, 3 h, 6 h and 12 h in RPMI 1640 culture media containing 10 % fetal cattle serum(FCS )(group A), 10% normal human serum (group B) and 10% MHD patient serum (group C) respectively. The immunocytochemical method was used to determine the expression of ICAM-1. Results: There were significant differences in the expression of ICAM-1 in HUVEC among stimulation groups with different serums(P < 0.05). Compared with groups A and B, the expression of ICAM-1 was significantly increased in HUVEC of group C. There was significant difference in the expression of ICAM-1 at the different stimulation times(P < 0.05). There was significant interaction between the expression of ICAM-1 in HUVEC and stimulation groups with different serum and the stimulation times(P < 0.05). Conclusion: The serum from MHD patients with chronic renal failure can promote the expression of ICAM-1 in HUVEC cultured in vitro, thus causing the dysfunction of endothelial cell.