肾缺血预处理对肾小管上皮细胞内钙超载的影响  

Protective Effects of Renal Ischemic Preconditioning on Calcium Overload in Renal Tubular Epithelia

作　　者：李荣山[1] 师梅[1] 

机构地区：[1]山西医科大学第二医院肾内科,太原030001

出　　处：《中国中西医结合肾病杂志》2008年第7期602-605,共4页Chinese Journal of Integrated Traditional and Western Nephrology

摘　　要：目的:通过观察肾缺血预处理(IPC)和缺血再灌注(I/R)过程中血清超氧化物歧化酶(SOD)、丙二醛(MDA)和细胞内游离钙离子浓度([Ca2+]i)含量的变化,进一步探讨肾IPC的保护机制。方法:将雄性SD大鼠88只随机分为11组,摘除右肾,分离并夹闭左肾动脉制备肾I/R和缺血预处理后缺血再灌注(IPC-I/R)动物模型。Ⅰa～Ⅴa(I/R)组为缺血再灌注0、1、24、48、72h组,Ⅰb～Ⅴb(IPC-I/R)组为缺血预处理后缺血再灌注0、1、24、48、72h组,Sham组为假手术组。比色法测定血清肌酐(Scr)、尿素氮(BUN)、SOD、MDA含量,流式细胞仪检测肾小管上皮细胞内[Ca2+]i水平,TUNEL原位标记法观察细胞凋亡情况。结果:除0h组外,IPC-I/R与I/R各组比较肾功能损害、细胞凋亡均明显减轻,SOD升高,MDA降低,[Ca2+]i水平下降;两种模型中均以再灌注24h组损伤最严重,Scr、BUN、MDA和[Ca2+]i水平最高,SOD水平最低,细胞凋亡最多;再灌注24h前损伤呈加重趋势,24h后逐渐减轻;组间比较,[Ca2+]i与血清SOD水平呈负相关,与MDA呈正相关。结论:肾IPC可以减轻I/R过程中膜脂质过氧化损伤和细胞内钙超载,从而减轻肾脏形态及功能损伤;膜脂质过氧化和细胞内钙超载相互作用,共同发挥对肾I/R损伤的保护作用。Objective： To observe the changes of serum superoxide dismutase（SOD）, malondialdehyde（MDA） and intracellular Ca^2＋ during renal ischemia/reperfusion（I/R） injury and ischemic preconditioning（ IPC）in order to explore the protective mech- anisms of renal IPC. Methods：Eighty - eight male SD rats were divided into 11 groups at random. Left renal arteries of I/R groups （ I a-- V a ） were clamped for 45 min after right kidneys was removed at 0,1, 24, 48 and 72 h after reperfusion. Rats in IPC - I/ R groups（ I b-- V b ）were preconditioned with renal ischemia by repeated clamping and unclamping of the left renal arteries before the operation. Sham operation was performed as control. Serum Scr, BUN, SOD and MDA levels were measured; Intracellular [ Ca2 ＋ ]i were assayed by a flow cytometry;Tubular apoptosis was detected by terminal dcoxynucleotidyl transferase（TdT） mediated dUTP- biotin nick- end labeling（TUNEL）. Results： Serum MDA and intracellular [ Ca2 ＋ ]i were significantly increased after renal I/R injury, while SOD level was markedly decreased after the injury. Renal I/R injury significantly increased apoptotic tubular cells with the peak at 24h after reperfusion. IPC reduced serum MDA and intracellular [Ca^2＋ ]i levels and increased SOD level. Also, IPC significantly inhibited tubular cell apoptosis. Conclusion： IPC can reduce the lipid peroxidation and attenuate intracellular calcium overload, thus it relieve renal injury during renal I/R;Lipid peroxidation and intracellular calcium overload prevented the kidney from injury. This may be partly the mechanisms of IPC＇ s renal protective effects.

关 键 词：缺血预处理 缺血再灌注 脂质过氧化 钙超载 凋亡 肾脏 

分 类 号：R692.6[医药卫生—泌尿科学]