摘要
目的:观察加味生脉散对大鼠缺血再灌注肾脏损伤的保护作用。方法:双侧肾动脉夹闭45min,再灌注24h,造成大鼠缺血再灌注肾脏损伤模型。分别测定加味生脉散治疗组、病理模型组、假手术组大鼠血尿素氮(BUN)、血肌酐(Cr)、组织中髓过氧物酶(MPO)和丙二醛(MDA)浓度,并进行组织病理学检查。结果:与病理模型组相比,加味生脉散治疗组的缺血再灌注大鼠血尿素氮下降42.8%(P=0.024),血清肌酐下降55.9%(P=0.011);肾脏组织MPO及MDA含量明显降低(P<0.01);组织病理学改变明显减轻(P<0.05)。结论:加味生脉散可减轻缺血再灌注引起的肾脏损伤,其机制与降低缺血再灌注有关的自由基损伤和炎性损伤有关。
Objective： To reveal the protective effect of Jia-wei Sheng-mai-san on renal ischemia-reperfusion injury in rats. Methods： Eighteen rats were divided randomly into three groups： group 1, sham operation; group 2, water （vehicle）-treated and group 3, Jia-wei Sheng-mai-san-treated. The rats in group 2 and group 3 were subjected to 45 min of warm renal ischemia and then received reperfusion for 24 h. At the same time, the rats in group 1 received sham operation. Three 3 days before renal ischemia operation, Jia-wei Sheng-mai-san was administrated to rats of group 3. Results：Rats administrated with Jia-wei Sheng-mai-san had less functional impairment of the kidneys than those in vehicle-treated group. The histological changes were not as severe as those of controls. Compared with vehicle-treated group, increases in serum creatinine and blood urea nitrogen 24 h after reperfusion were attenuated by 55.9% （ P = 0.011 ） and by 42. 8% （P =0. 024）, respectively in group 3. The ischemia-reperfusion-induced increases in tissue myeloperoxidase （MPO）and malondialdehyde（MDA） were reduced by 68% （P 〈 0. 001 ） and 59% （ P 〈 0. 001 ） respectively in group 3. Tubular cell necrosis in medulla was less pronounced （ P 〈 0.05 ） in animals administrated with Jia-wei Sheng-mai-san. Condusion： Jia-wei Sheng-mai-san could partly mitigate renal damage or failure after ischemia-reperfusion injury of the kidney by inhibition of neutrophil infiltration and oxidation injury.
出处
《军事医学科学院院刊》
CSCD
北大核心
2005年第4期346-348,共3页
Bulletin of the Academy of Military Medical Sciences
关键词
急性肾小管坏死
缺血再灌注损伤
加味生脉散
大鼠
acute tubular necrosis
ischemia-reperfusion injury
Jia-wei Sheng-mai-san
rats
作者简介
李静（1973-），女，河北省阜城县人，硕士，医师。
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