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：

江曉琴1，倪娟1，楊沛2，羅金鳳1，黃蔚1，李華鳳1

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【摘要】目的 探討急性腎缺氧復氧損傷過程中氧化侵襲與腎細胞凋亡在腎損傷發生機制中的作用。方法 20只雄性新西蘭大白兔隨機分成兩組，每組10只。正常對照組（A組）：吸入空氣6 h。單純缺氧復氧組（B組）:經自制面罩吸入8% O2 3 h，缺氧結束后吸入空氣復氧3 h，制成全身缺氧復氧模型。復氧結束后立即處死動物，取出腎臟組織，一份行HE染色，觀察組織病理學改變，一份供半胱氨酸蛋白酶3（caspase-3）檢測，一份供檢測丙二醛（MDA）、超氧化物歧化酶（SOD）。結果病理學檢查結果顯示，A組腎臟組織結構基本正常，未見病理性改變，腎臟組織中極少的caspase-3陽性細胞表達。B組:腎小管上皮細胞腫脹，空泡變性；可見少量壞死，管腔明顯擴張；caspase陽性蛋白表達指數（29.3±5.7）%。B組和A組MDA分別為（28.05±1.92）、（7.88±1.69）nmol/g；SOD分別為（218±18.41）、（372±13.14）U/g，兩組比較，均有統計學意義（P lt;0.05）。結論兔腎臟缺氧復氧損傷與氧化侵襲與細胞凋亡密切相關。
【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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