[1]陈贝贝,王亮,崔洁,等.不同缺血预处理对CO2气腹模型大鼠肾脏缺血再灌注损伤的影响[J].陆军军医大学学报(原第三军医大学学报),2015,37(20):2032-2037.
 Chen Beibei,Wang Liang,Cui Jie,et al.Effect of ischemic preconditioning on kidney ischemia/reperfusion injury induced by CO2 pneumoperitoneum in rats[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(20):2032-2037.
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
37卷
期数:
2015年第20期
页码:
2032-2037
栏目:
论著
出版日期:
2015-10-30

文章信息/Info

Title:
Effect of ischemic preconditioning on kidney ischemia/reperfusion injury induced by CO2 pneumoperitoneum in rats
作者:
陈贝贝王亮崔洁叶茂唐文
重庆医科大学附属儿童医院麻醉科,儿童发育疾病研究省部共建教育部重点实验室,儿科学重庆市重点实验室,重庆市儿童发育重大疾病诊治与预防国际科技合作基地
Author(s):
Chen Beibei Wang Liang Cui Jie Ye Mao Tang Wen

Department of Anesthesiology, Key Laboratory of Developmental Diseases in Childhood of Ministry of Education, Chongqing Key Laboratory of Pediatrics, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, 400014, China

关键词:
缺血预处理缺血/再灌注损伤CO2气腹细胞凋亡氧化应激
Keywords:
ischemic preconditioning ischemia/reperfusion injury CO2 pneumoperitoneum apoptosis oxidative stress
分类号:
R-332;R459.9;R692.05
文献标志码:
A
摘要:

目的      探讨不同缺血预处理对CO2气腹模型大鼠肾脏缺血再灌注损伤的影响及其有关机制。      方法      将30只雄性SD大鼠分为5组(n=6):假手术对照(Sham)组,气腹(Pp)组,缺血预处理1次(IP1)组,缺血预处理3次(IP3)组,缺血预处理5次(IP5)组。对照组接受假手术,其余各组以10 mmHg 气腹压力建立CO2气腹模型,持续时间60 min,IP1、IP3、IP5组在气腹前以10 mmHg压力,充气5 min放气 5 min,分别连续1、3、5次;恢复灌注60 min后光镜下观察各组肾组织病理形态学变化,检测肾脏组织匀浆丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性及总抗氧化能力(T-AOC)变化;免疫组织化学和Western blot方法检测Bcl-2和Bax蛋白在肾组织中的表达。      结果      大鼠肾组织病理形态学显示,Pp组肾小管上皮细胞水肿、变性坏死,管腔扩张,间质炎症细胞浸润,而各IP组肾损伤程度明显减轻;与Sham组相比,Pp组及各IP组肾组织匀浆MDA含量显著升高,SOD和T-AOC活性显著下降(P<0.05);与IP1组相比,IP3组MDA含量下降,SOD、T-AOC活性升高(P<0.05),IP3、IP5组间差异无统计学意义(P>0.05);免疫组织化学和Western blot结果显示: 与Sham组比较,Pp组Bcl-2、Bax蛋白的表达均升高,而Bcl-2/Bax比值显著降低(P<0.05);与IP1、IP5组相比,IP3组Bcl-2表达升高,Bax表达下降,Bcl-2/Bax比值显著升高(P<0.05)。      结论      缺血预处理可以减轻CO2气腹大鼠肾脏缺血再灌注损伤,其中预处理3次对减轻缺血/再灌注肾组织损伤作用更明显,其机制可能与直接降低氧化应激反应活性氧的生成,上调Bcl-2抗凋亡蛋白表达,下调Bax凋亡蛋白表达有关。

Abstract:

Objective      To investigate the effect of ischemic preconditioning on CO2 pneumoperitoneum-induced kidney ischemia/reperfusion injury in rats and related mechanism.       Methods      Thirty male SD rats were divided into 5 groups (n=6): sham group, pneumoperitoneum (Pp) group, ischemic preconditioning group for 1 cycle (IP1), ischemia preconditioning group for 3 cycles (IP3), and ischemic preconditioning group for 5 cycles (IP5). The sham group was subjected to sham operation, and the other groups were subjected to CO2 Pp for 60 min under 10 mmHg intra-abdominal pressure. IP1, IP3 and IP5 groups were subjected to preconditioning prior to Pp/deflation through 5 min of Pp, immediately followed by 5 min of deflation, for 1, 3, and 5 cycles, respectively. After deflation for 60 min, the kidney pathological changes were observed with light microscopy. Kidney tissue samples were taken for measuring malondialdehyde (MDA), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC). The expression of Bcl-2 protein and Bax protein was determined by immunohistochemistry and Western blotting.       Results      Microscopic examination showed the edema, degeneration and necrosis of renal tubule endothelial cells, tubular ectasia, congestion, and infiltration of neutrophils in the Pp group. Histological damage of renal tubules in the IP1, IP3, and IP5 groups was much milder than that in the Pp group (P<0.05). Compared with the Pp group, the kidney MDA levels were remarkably decreased in the IP1, IP3 and IP5 groups, whereas the kidney SOD and T-AOC contents were increased significantly (P<0.05). Immunohistochemical staining and Western blotting results showed that, compared with the Pp group, the expression of Bcl-2 protein was increased and that of Bax protein was decreased in the IP3 group (P<0.05).       Conclusion      Ischemic preconditioning may decrease renal ischemia/reperfusion injury induced by CO2 Pp in the rats, and ischemic preconditioning for 3 cycles is most effective. The mechanism may be associated with the decrease of oxygen free radicals, up-regulated expression of Bc1-2 protein and down-regulated expression of Bax protein.

相似文献/References:

[1]唐维平,司良毅,张乐之,等.大鼠心肌缺血再灌注损伤时细胞核游离钙浓度的变化[J].陆军军医大学学报(原第三军医大学学报),2005,27(02):112.

更新日期/Last Update: 2015-10-22