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机构地区:[1]上海交通大学附属第六人民医院外科,上海200233
出 处:《中国临床医学》2006年第1期84-86,共3页Chinese Journal of Clinical Medicine
基 金:国家自然科学基金(批准号30271286)上海市科委青年科技启明星跟踪计划(批准号02QMB1406)资助项目
摘 要:目的:探讨细胞钙含量、肠上皮细胞(intestinal epithelial cell,IEC)缺血缺氧损伤及钙离子阻断剂对凋亡的影响。方法:采用体外表衬人工细胞基底膜原代培养胎鼠IEC,建立缺血缺氧环境后,实验组分为对照组(A组),模拟缺氧组(B 组),模拟缺血组(C组),模拟缺氧缺血组(D组)及加入维拉帕米后的相应对照组A2组,B2组,C2组,D2组;观察细胞内钙含量及IEC脱落、凋亡率。结果:损伤组细胞内钙超载,尤以D1组细胞内钙超载最显著(P<0.01),其次为B1组(P <0.01),C1组(P<0.05);加用钙通道阻断剂后细胞内钙含量下降与相应对照组相比以D2组最明显(P<0.01),依次为 B2(P<0.01)、C2(P<0.05);各组凋亡率也相应下降,尤以D2组下降更显著。结论:细胞内钙超载与IEC脱落、凋亡密切相关,钙离子阻断剂降低细胞内钙超载,达到减少细胞凋亡脱落。Objective: To study the influence on the IEC apoptosis with ischemia and anoxia injury, and the relationship of intracellular calcium amount and the effects of calcium channel amagonist on apoptosis. Methods: Construction of model of IEC apoptosis induced by ischemia and anoxia, IECs were divided into eight groups, namely, A1 (control group), B1 (anoxia group) ,C1(ischemia group) ,D1(ischemia and anoxia group) ; A2 (A1 + 2mg/1 verapanil group), B2.(B1 + 2mg/ 1 verapanil), C2(C1 + 2mg/l verapanil), D2 (D1 + 2mg/l verapanil), The apoptosis rate was determined by FCM, intracellular calcium amount was measured by LSCM. Results. The Intracellular calcium and the apoptosis rate (AR) increased in B1 ,C1 ,D1 group as compared with group A1, P〈0. 01 ,AR in group D was higher than that in group B1 ,C1, P〈0, 05 ; The AR were inhibited and decreased after using the calcium channel antagonist (verapanil), and the AR in group 152 improved markedly as compared with other groups. Condusion:Intracellular culcium overload is relative to the apoptosis of IEC under ischemia and anoxia; calcium channel amagonist (verapanil) could decrease intracellular calcium and apoptosis rate of IEC.
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