中文摘要：

目的 探讨重组人肝再生增强因子（ rhALR）对缺血再灌注（IR）肾损伤大鼠模型肾脏局部炎性细胞浸润及炎性因子表达的影响.方法 将SD大鼠按随机数字表法分成假手术组、IR组、rhALR低剂量（100 μg/kg）组及rhALR高剂量（200 μg/kg）组.采用双侧肾蒂夹闭60 min后再灌注建立IR肾损伤动物模型.常规生化法检测血肌酐、尿素氮的水平,HE染色观察肾脏组织学改变,比色法检测肾组织髓过氧化物酶（ MPO）的活性,Western印迹法检测肾组织肿瘤坏死因子α（TNF-α）、细胞间黏附分子1（ICAM-1）、单核细胞趋化蛋白1（MCP-1）的蛋白表达.结果 rhALR组的血肌酐和尿素氮显著低于IR组（均P＜ 0.05）,肾组织病理损害减轻,rhALR高剂量组较rhALR低剂量组肾功能及肾脏病理改善更明显.IR组大鼠肾组织的MPO活性、TNF-α、ICAM-1、MCP-1的蛋白表达在术后12 h较假手术组显著上升,术后24h有所下降,但仍维持在较高水平（均P＜0.05）；rhALR组肾组织MPO活性、肾组织TNF-α、ICAM-1、MCP-1的蛋白表达较IR组显著下降（均P＜0.05）,且rhALR高剂量组4者较rhALR低剂量组下降更显著（均P＜0.05）.结论 rhALR对IR肾损伤具有保护作用,其作用机制可能与其减少肾脏局部的炎性细胞浸润、抑制炎性因子MCP-1、ICAM-1、TNF-α的表达有关.

英文摘要：

Objective To investigate the effects of recombinant human augmenter of liver regeneration （rhALR） on renal inflammation in acute kidney injury （AKI） induced by renal ischemia reperfusion （IR）. Methods SD rats were randomly divided into sham-operated group,IR group,rhALR1 group （100 μg/kg） and rhALR2 group （200 μg/kg）.Both renal pedicles of rats were identified and occluded with microvascular clamps for 60 min to induce acute kidney injury （AKI）.Blood urea nitrogen and serum creatinine levels were evaluated using a Hitachi 747 automatic analyzer. For histological examination, sections were stained with HE. The activity of myeloperoxidase （MPO） was detected by spectrophotometer.Expression of TNF-α,ICAM-1,MCP-1 was determined by Western blotting. Results Blood urea nitrogen,serum creatinine levels and the injury of kidney were improved significantly in rhALR group as compared with IR group （all P〈 0.05）.They were improved more significantly in rhALR2 group as compared to in rhALR1 group （all P〈0.05）.The protein levels of TNF-α,ICAM-1,MCP-1 and the activity of MPO in kidneys from the sham-operated rats were low,and increased significantly after renal ischemia reperfusion injury （all P〈0.05）.After treated with rhALR,the expression of TNF-α,ICAM-1,MCP-1 and the activity of MPO were decreased significantly in kidneys as compared to those in IR group （all P〈0.05）,which decreased more significantly in rhALR2 group than those in rhALR1 group （all P〈 0.05）. Conclusions nhALR can protect kidneys from ischemia reperfusion injury in rats.The mechanism may be associated with the inhibition of renal inflammatory cells infiltration and down-regulated expressions of YNF-α,ICAM-1 and MCP-1 in the kidney.