缺血后处理对大鼠肾缺血/再灌注损伤及p38MAPK活性的影响  

Effects of Ischemic Postconditioning on Ischemia Reperfusion Injury and Expression of p38MAPK Protein in Rat Kidney

作　　者：李涛[1] 王雪岩[2] 姜秀良[1] 梁立升[1] 李爱芝[1] 马宏仲[1] 马加海[1] 

机构地区：[1]青岛大学医学院附属烟台毓璜顶医院麻醉科,山东烟台264000 [2]烟台市疾病预防控制中心,山东烟台264000

出　　处：《医学综述》2015年第11期2049-2051,共3页Medical Recapitulate

基　　金：烟台市科技发展计划项目(2009155-12)

摘　　要：目的研究缺血后处理(IPO)对大鼠肾缺血/再灌注损伤(IRI)及p38丝裂原活化蛋白激酶(p38MAPK)活性的影响。方法将24只SD大鼠依据随机数字表法分为3组,各8只。对照(S)组:仅结扎右侧肾蒂,左肾蒂游离;缺血/再灌注(IR)组:结扎右侧肾蒂,夹闭左侧肾蒂60 min后,开放灌注24 h;IPO组:肾脏缺血60 min后,进行10 s灌注、10 s阻断,共6个循环的IPO,然后开放灌注24 h,余同IR组。检测血尿素氮(BUN)、肌酐,酶联免疫吸附试验法检测肾组织肿瘤坏死因子α(TNF-α)、白细胞介素1(IL-1)水平,Western blot法检测肾组织磷酸化p38MAPK蛋白表达,观察肾组织的病理学变化。结果与S组比较,IR组和IPO组血BUN、肌酐,肾TNF-α、IL-1、p38MAPK蛋白表达量及组织病理评分显著增加(P<0.05);IPO组各指标较IR组显著下降(P<0.05)。结论 IPO能减轻肾IRI,其机制与抑制p38MAPK活化,进而抑制炎性因子释放有关。Objective To investigate the effects of ischemic postconditioning on ischemia reperfusion injury（ IRI） and expression of p38 mitogen-activated protein kinase （ p38MAPK） protein in rat kidney. Methods A total of 24 SD rats were allocated randomly into 3 groups（n=8 per group）.Sham （S） group：rats received continuous intravenous infusion of normal saline and clamping the right renal pedicles .IR group （ IR）：renal IRI was induced by clamping both renal pedicles 60 minutes followed by 24 h reperfusion.Ische-mic postconditioning（IPO） group：ischemic postconditioning was given six cycles of 10 s reperfusion/10 s occlusion followed by 24 h reperfusion.Serum blood urea nitrogen（BUN）, creatinine（Cr） was detected. ELISA was used to detect the tumor necrosis factorα（TNF-α）,interleukin 1 （IL-1） in kidney.Western blot was applied to detect the expression of p38MAPK protein.Renal histopathology lesions were also examined. Results Compared with group S,the serum BUN and Cr,renal TNF-αand IL-1,expression of p38MAPK protein increased significantly in group IR and group IPO（P〈0.05）.Compared with group IR,all indexes in group IPO decreased significantly（P 〈0.05）.Conclusion IPO can attenuate renal IRI in rats.The mechanism is related to inhibition of p38MAPK expression and inflammatory factor release.

关 键 词：缺血/再灌注损伤 肾脏 缺血后处理 P38丝裂原活化蛋白激酶 

分 类 号：R692.9[医药卫生—泌尿科学]