CAJ | 학술논문

【目的】探讨血肌酐(SCr)、尿素氮(BUN)在小鼠肾脏缺血再灌注损伤(IRI)中的表达及其意义。【方法】以雄性 C57BL/6J 小鼠为研究对象,随机分为小鼠肾脏 IRI 模型(IR 组)、假手术模型(S 组)和对照组(C 组),检测各组小鼠不同时间点 SCr、BUN 水平,并分析其肾组织及肺组织病理损害程度。【结果】C 组、S组不同时间点 SCr 及 BUN 水平比较无显著差异(P >0.05),IR 组在再灌注后0 h 至7 d 呈逐渐升高而后降低的趋势,24 h 达到峰值。C 组、S 组不同时间点肾小管间质损伤及肺病理损伤评分比较均无显著差异(P >0.05),在 IR 组同样表现为先升高而后降低的趋势,肾小管间质损伤病理评分于再灌注24 h 达到最高峰,肺脏病理损害及评分在48~72 h 达到最高峰。【结论】小鼠肾脏 IRI 模型是稳定的急性肾损伤(AKI)模型,建模成功率高；缺血性 AKI 可诱导肺部的炎症反应,诱发急性肺损伤(ALI)。
【목적】탐토혈기항(SCr)、뇨소담(BUN)재소서신장결혈재관주손상(IRI)중적표체급기의의。【방법】이웅성 C57BL/6J 소서위연구대상,수궤분위소서신장 IRI 모형(IR 조)、가수술모형(S 조)화대조조(C 조),검측각조소서불동시간점 SCr、BUN 수평,병분석기신조직급폐조직병리손해정도。【결과】C 조、S조불동시간점 SCr 급 BUN 수평비교무현저차이(P >0.05),IR 조재재관주후0 h 지7 d 정축점승고이후강저적추세,24 h 체도봉치。C 조、S 조불동시간점신소관간질손상급폐병리손상평분비교균무현저차이(P >0.05),재 IR 조동양표현위선승고이후강저적추세,신소관간질손상병리평분우재관주24 h 체도최고봉,폐장병리손해급평분재48~72 h 체도최고봉。【결론】소서신장 IRI 모형시은정적급성신손상(AKI)모형,건모성공솔고；결혈성 AKI 가유도폐부적염증반응,유발급성폐손상(ALI)。
[Objective]To investigate the occurrence and progress of serum creatinine and urea nitrogen in ischemia-reperfusion of mice kidney injury.[Methods]Male mice (C57BL/6J)used as subjects were randomly distributed in three groups:the ischemia-reperfusion group (IR),the sham surgery group (S)and the control group (C),and the SCr and UN levels of the 3 groups at different time points and the their kidney/lung tissue pathological damage were detected and analyzed.[Results]Levels of SCr and UN showed no significant differ-ence in the Group C and the Group S (P >0.05).From 0h to 7d following reperfusion,the SCr and UN levels gradually increased and then decreased,and reached the peak value 24h after reperfusion .The interstitial dam-age score of renal tubules and pathological damage score of lung injury at different time points presented com-paratively no significant difference between group C and group S (P >0.05).The IR Group presents the same tendency ,increasing first ,than decreasing ,the pathological grading of renal tubular interstitial injury reached the peak value 24h after reperfusion;Pathological damage score of lung injury reached the peak value in 48~72 h.[Conclusion]The mice model of ischemia-reperfusion renal injury is one steady animal model for research of Acute kidney injury(AKI),and ischemia AKI may induce pulmonary inflammatory reaction,and bring out a-cute kidney injury(AKI)as well.