摘要
目的探讨二氧化碳气腹后致大鼠肾脏缺血再灌注损伤，以及异丙酚在缺血再灌注损伤过程中的保护作用机制。方法成年雄性Wistar大鼠48只，体重280～320g，实验前12h禁食，自由饮水，采用随机数字表法将大鼠随机分为对照组、缺血组及再灌注组和异丙酚组，每组12只。对照组未经任何处理，仅经尾静脉泵注生理盐水1h[10ml／（kg．h）]；缺血组在对照组的基础上，给予20mmHg（1mmHg=0．133kPa）气腹压力1h；再灌注组在缺血组的基础上，放开气腹压力后持续0．5h；异丙酚组给予20mmHg气腹压力1h，放开气腹压力后持续0．5h，经尾静脉泵注异丙酚10ml／（kg．h）（生理盐水10倍稀释）。观察各组尿素氮（bloodureanitrogen，BUN）、肌酐（creatinine，Cr）、超氧化物歧化酶（superoxidedismutase，SOD）、丙二醛（malondialdehyde，MDA）、核因子E2相关因子（nuclearfactorE2-relatedfactor2，Nrf2）表达的变化。结果对照组、缺血组、再灌注组的BUN、Cr、MDA水平逐渐增高，SOD水平逐渐降低（P均〈0．05）；与缺血组及再灌注组比较，异丙酚组的BUN、Cr、MDA水平明显降低，SOD水平明显增高（P均〈0．05）。Nrf2蛋白及mRNA在对照组、缺血组、再灌注组、异丙酚组中的表达逐渐增加（P均〈0．05）。结论二氧化碳气腹对大鼠。肾脏造成缺血再灌注损伤；异丙酚可通过调节Nrf2蛋白的表达，对大鼠肾脏缺血再灌注损伤产生保护作用。
Objective To investigate the mechanism of renal ischemia reperfusion injury （IRI） caused by carbon dioxide pneumoperitoneum, and to discuss the protective effect of propofol in rats. Methods Forty-eight male Wistar rats, weighing 280 to 320 g, were selected and prepared by fasting but free drinking for 12 hours before the experiment. They were randomly divided into four groups by random number table （ 12 rats in each group） ：control group, ischemic group, reperfusion group and propofol group. Control group： normal saline infusion[ 10 ml/（kg.h） ] for 1 h in caudal vein without any other treatment. Ischemic group：on the basis of control group, supply with 20 mmHg （ 1 mmHg = 0. 133 kPa） pneumoperitoneum pressure for 1 h. Reperfusion group：on the basis of ischemic group, keep pneumoperitoneum pressure open for 30 min. Propo- fol group：infusion propofol in caudal vein [ 10 ml/（ kg. h）, saline 10-fold dilution ], given 20 mmHg pneu- moperitoneum pressure for 1 h, then kept this pressure open for 30 min. The expression changes of blood urea nitrogen（ BUN）, creatinine （ Cr）, superoxide dismutase （ SOD）, malondialdehyde （MDA） and nuclear factor E2-related factor 2 （Nrf2） were detected individually. Results The levels of BUN, Cr and MDA gradually increased,while the level of SOD decreased in control group, ischemic group and reperfusion group （P 〈 0. 05, respectively）. Compared with ischemic group and reperfusion group, the levels of BUN, Cr and MDA decreased significantly, and the level of SOD increased markedly in propofol group （P 〈 0. 05, respectively）. The expression of Nrf2 protein and mRNA gradually increased in the control group,ischemia group,reperfu- sion group and propofol group （P 〈 0. 05 ）. Conclusion Carbon dioxide pneumoperitoneum can cause renal IRI in rats. Propofol has a protective effect of IRI by regulating the expression of Nrf2 protein.
出处
《中国小儿急救医学》
CAS
2016年第1期33-36,共4页
Chinese Pediatric Emergency Medicine
关键词
二氧化碳
缺血再灌注损伤
肾脏
异丙酚
核因子E2相关因子
Carbon dioxide
Ischemia reperfusion injury
Kendy
Propofol
Nuclear factor E2-related factor 2
