【摘要】 目的探讨芪归益肾方对缺血再灌注致急性肾损伤小鼠的保护作用。方法 ICR小鼠随机分成假手术组、模型组、芪归益肾方组(50 g/kg)和硫辛酸组(硫辛酸0.1 g/kg)。各组灌胃处理1周后,利用肾动脉夹闭及恢复血流建造肾缺血再灌注损伤模型,造模24 h后采集全血,分离肾脏组织。全自动生化分析仪检测血清肌酐(Scr)、尿素氮(BUN)水平,试剂盒检测超氧化物歧化酶(SOD)活性、丙二醛(MDA)水平,HE染色、免疫组化和Western blot观察肾脏组织形态学变化和检测HO-1、Nrf2表达。结果除假手术组外,其余各组小鼠血清Scr、BUN水平和肾组织肾小管损伤评分均升高,但均低于模型组(P<0.05)。HE染色显示除假手术组外,其余各组存在不同程度的肾小管损伤,而药物干预组病理损伤较模型组减轻(P<0.05),其中芪归益肾方组最明显。免疫组织化学和Western blot结果表明,芪归益肾方和硫辛酸组小鼠MDA水平低于模型组,而SOD活性及HO-1、Nrf2表达高于模型组(P<0.05)。结论芪归益肾方可通过调控Nrf2/HO-1通路,基于抗氧化机制对缺血再灌注诱导的急性肾损伤小鼠肾脏组织发挥保护作用。更多还原

【Abstract】 AIM To investigate the protective effects of Qigui Yishen Formula on acute renal injury induced by ischemia-reperfusion in mice. METHODS ICR mice were randomly divided into sham operation group, model group, Qigui Yishen Formula group(50 g/kg) and lipoic acid group(0.1 g/kg). After one week of intragastric administration, the renal ischemia-reperfusion injury model was established by clamping the renal artery and restoring the blood flow. Twenty-four hours after the model establishment, the collected mouse whole blood and the procured renal tissue were subjected to the detection of levels of serum creatinine(Scr), urea nitrogen(BUN) by automatic biochemical analyzer; determination of their activity of superoxide dismutase(SOD) and level of malondialdehyde(MDA) by test kits; the observation of the renal histomorphological changes by HE staining; and the identification of the expressions of HO-1 and Nrf2 by immunohistochemistry and Western blot. RESULTS Except for the sham operation group, the other groups shared increased serum Scr and BUN levels, and the scores of renal tubular injury, among which the model group displayed its inferiority(P<0.05). The results of immunohistochemistry and Western blot showed lower MDA level, higher SOD activity and improved expressions of HO-1 and Nrf2 in groups of Qigui Yishen Formula and lipoic acid than the model group(P<0.05). CONCLUSION Qigui Yishen Formula can protect the kidney tissue of mice with acute renal injury induced by ischemia-reperfusion based on antioxidant mechanism via Nrf2/HO-1 pathway regulation.更多还原