[1]冀志勇,景宇,张建国,等.内质网应激预处理对大鼠急性缺血性肾损伤的保护作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(12):1253-1256.
 Ji Zhiyong,Jing Yu,Zhang Jianguo,et al.Endoplasmic reticulum stress pretreatment protects acute ischemic kidney injury in rats[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(12):1253-1256.
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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:
32卷
期数:
2010年第12期
页码:
1253-1256
栏目:
论著
出版日期:
2010-06-30

文章信息/Info

Title:
Endoplasmic reticulum stress pretreatment protects acute ischemic kidney injury in rats
作者:
冀志勇景宇张建国李开龙詹俊林利容何娅妮
第三军医大学大坪医院野战外科研究所肾内科
Author(s):
Ji Zhiyong Jing Yu Zhang Jianguo Li Kailong Zhan Jun Lin Lirong He Yani
Department of Nephrology, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, 400042, China
关键词:
损伤再灌注损伤内质网应激大鼠
Keywords:
kidney reperfusion injury endoplasmic reticulum stress rats
分类号:
R364.12;R692;R983
文献标志码:
A
摘要:
目的    研究内质网应激预处理对大鼠急性缺血性肾损伤的保护作用。    方法    24只雄性SD大鼠均分为对照组、衣霉素(tunicamycin,TM)处理组、缺血再灌注(ischemia reperfusion,I/R)组,衣霉素+缺血再灌注(TM+I/R)组。采用自动生化分析仪检测大鼠血肌酐、尿素氮水平, PAS染色检测肾小管损伤情况,免疫组化和Western blot检测肾组织内质网应激标志物GRP78蛋白表达。    结果    ①与对照组(0.2±0.03)比较,I/R组肾组织GRP78表达(2.4±0.17)增加(P<0.05),与对照组血肌酐、尿素氮[(47.42±6.02)μmol/L、(4.75±1.77)mmol/L]比较,I/R组血肌酐[(186.83±20.21)μmol/L]、尿素氮[(21.73±2.33)mmol/L]水平升高(P<0.05),肾小管损伤评分升高。     ②TM组大鼠肾组织GRP78表达升高,但未见明显肾小管损伤,与对照组比较,血肌肝、尿素氮水平无明显变化。     ③与I/R组比较,TM+I/R组大鼠GRP78表达(3.2±0.24)升高;肾小管损伤评分降低(P<0.05),血肌酐[(98.72±14.55) μmol/L]、尿素氮[(13.22±2.45)mmol/L]水平降低(P<0.05)。    结论    内质网应激预处理对急性缺血性肾损伤有保护作用,其机制可能为通过激活适宜的内质网应激,上调肾组织GRP78表达,从而抑制I/R导致的过度内质网应激,提高肾组织对缺血的耐受性,减轻细胞和组织损伤,实现其对大鼠急性缺血性肾损伤的保护作用。
Abstract:
Objective    To observe the protection and underlying mechanism of preconditioning with endoplasmic reticulum stress (ERS) by tunicamycin on rat acute ischemic kidney injury.     Methods    Twenty-four SD rats were divided into 4 groups randomly, sham operation group, tunicamycin group , ischemia reperfusion (I/R) group, tunicamycin pretreatment + I/R group. The renal ischemia and reperfusion model was developed by bilateral clamping of the renal pedicle for 40 min and then reperfusing for 12 h. Tunicamycin was intraperitoneally administered to rats 24 h prior to I/R at a dosage of 0.6 mg/kg. Serum creatinine (SCr) and blood urea nitrogen (BUN) were detected with automatic biochemistry analyzer. Renal tubular injury was measured by PAS staining in the kidney tissue samples at 36 h after operation and evaluated with kidney tubules scoring. The expression of GRP78 in the ischemic renal tissue was detected by Western blotting and    immunohistochemical assay.     Results    Compared with sham operation group(0.20±0.03), the expression of GRP78 protein was increased significantly in I/R group(2.40±0.17, P<0.05), and the levels of SCr and BUN were increased significantly in this group [(186.83±20.21)μmol/L,(21.73±2.33)mmol/L] compared with sham operation group[(47.42±6.02)μmol/L,(4.75±1.77)mmol/L] (P<0.05). I/R group had a higher kidney tubule score than sham operation group (3.69±0.45 vs 0, P<0.05). Tunicamycin induced the expression of GRP78 protein to elevate but had no effect on SCr and BUN, or kidney tubule injury. Compared with I/R group, the expression of GRP78 protein of TM+I/R group(3.2±0.24) was increased(P<0.05), The levels of SCr, BUN were decreased significantly in TM+I/R group[(98.72±14.55) μmol/L and(13.22±2.45)mmol/L] compared with I/R group(P<0.05),and the score of renal tubular injury was decreased significantly in TM+I/R group(2.45±0.33) compared with I/R group(3.69±0.45) (P<0.05).     Conclusion    Pretreatment with ERS protects the rats from acute ischemic kidney injury. The mechanism may be through activating ERS and up-regulating the expression of GRP78, then inhibiting the excessive ERS and increasing the kidney tolerance to ischemia and alleviating cellular and tissue injury. In this way, pretreatment with ERS exerts a protective effect against renal ischemia reperfusion injury.

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更新日期/Last Update: 2010-06-22