Relationship of Acute Renal Hypoxic-reoxygenation Injury with Oxidative Invasion and Cellular Apoptosis in Rabbits_West China Medical Journal

Authors：

JIANG Xiaoqin ¹ ,  NI Juan ¹

Department of Anesthesiology, West China Second Hospital, Sichuan University, Chengdu, Sichuan 610041, P. R. China;

Corresponding author：

NI Juan, Email: angeljxq@yahoo.com.cn

Keywords：

江晓琴1，倪娟1，杨沛2，罗金凤1，黄蔚1，李华凤1

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【摘要】目的 探讨急性肾缺氧复氧损伤过程中氧化侵袭与肾细胞凋亡在肾损伤发生机制中的作用。方法 20只雄性新西兰大白兔随机分成两组，每组10只。正常对照组（A组）：吸入空气6 h。单纯缺氧复氧组（B组）:经自制面罩吸入8% O2 3 h，缺氧结束后吸入空气复氧3 h，制成全身缺氧复氧模型。复氧结束后立即处死动物，取出肾脏组织，一份行HE染色，观察组织病理学改变，一份供半胱氨酸蛋白酶3（caspase-3）检测，一份供检测丙二醛（MDA）、超氧化物歧化酶（SOD）。结果病理学检查结果显示，A组肾脏组织结构基本正常，未见病理性改变，肾脏组织中极少的caspase-3阳性细胞表达。B组:肾小管上皮细胞肿胀，空泡变性；可见少量坏死，管腔明显扩张；caspase阳性蛋白表达指数（29.3±5.7）%。B组和A组MDA分别为（28.05±1.92）、（7.88±1.69）nmol/g；SOD分别为（218±18.41）、（372±13.14）U/g，两组比较，均有统计学意义（P lt;0.05）。结论兔肾脏缺氧复氧损伤与氧化侵袭与细胞凋亡密切相关。
【Abstract】 Objective To investigate the effect of oxidative invasion and cellular apoptosis on the mechanism of kidney injury during the process of acute renal hypoxic-reoxygenation injury. Methods Twenty male white New Zealand rabbits were selected and randomly divided into two groups with 10 rabbits in each. The rabbits in normal control group inhaled air for 6 hours while the ones in hypoxic/reoxygenation (H/R) group breathing in air for 3 hours inhaled 8% O2 for 3 hours after. After the H/R mode was set up, the rabbits were executed, and the kidney tissues were removed in which the caspase-3 protein expression was assessed by immunohistochemical method. Superoxide dismutase (SOD) activity and malonical aldehyde (MDA) were also detected. Results The results of pathological examination showed that the structure of renal tissues was normal with little expression of caspase-3; while swelling of renal tubular epithelial cells, vacuolar degeneration, little necrosis, dilated vascular lacuna were found in H/R group. The positive expression of caspase-3 was (29.3±5.7)% in H/R group. The contents of MDA were (28.05±1.92) and (7.88±1.69) nmol/g and SOD were (218±18.41) and (372±13.14) U/g in H/R and control group, respectively; the differences between the two groups were significant (P lt;0.05). Conclusion The acute renal hypoxic/reoxygenation injury has a correlation with oxidative invasion and cellular apoptosis.

Citation： JIANG Xiaoqin,NI Juan,YANG Pei,LUO Jinfeng,HUANG Wei,LI Huafeng. Relationship of Acute Renal Hypoxic-reoxygenation Injury with Oxidative Invasion and Cellular Apoptosis in Rabbits. West China Medical Journal, 2010, 25(10): 1841-1843. doi: Copy

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1. Perico N, Catanneo D, Sayegh M, et al. Delayed graft function in kidney transplantation Lancet[J]. 2004, 364(9447): 1814-1827.
2. Aronson S, Blumenthal R, et al. Perioperative renal dysfunction and cardiovascular anesthesia: concerns and controversies[J]. J cardiothorac Vasc Anesth, 1998, 12(5): 567-586.
3. Vianna PT, Castiglia YM, Braz JR, et al. Remifentanil, isoflurane, and preconditioning attenuate renal ischemia/reperfusion injury in rats[J]. Transplant Proc, 2009, 41(10): 4080-4082.
4. Wang Y, Ji HX, Zheng JN, et al. Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1-MKK3-p38 signal pathway[J]. Redox Rep, 2009, 14(6): 243-250.
5. Yang CC, Lin LC, Wu MS, et al. Repetitive hypoxic preconditioning attenuates renal ischemia/reperfusion induced oxidative injury via upregulating HIF-1 alpha-dependent bcl-2 signaling[J]. Transplantation, 2009, 88(11): 1251-1260.
6. Yuste VJ, Sanchez-Lopez I, Sole C, et al. The contribution of apoptosis inducing factor, caspase-activated DNase, and inhibitor of caspase-activated Dnase to the nuclear phenotype and DNA[J]. J Biol Chem, 2005, 280(42): 35670-35683.
7. Shelley X, Zhang L, James J, et al. Whole-body hypoxic preconditioning protects mice against acute hypoxia by improving lung function[J]. J Appl Physiol, 2004, 96(1): 392-397.

West China Medical Journal

Relationship of Acute Renal Hypoxic-reoxygenation Injury with Oxidative Invasion and Cellular Apoptosis in Rabbits

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