Effects of recombinant human augmenter of liver regeneration on renal inflammation after renal ischemia reperfusion injury in rats
10.3760/cma.j.issn.1001-7097.2012.02.008
- VernacularTitle:肝再生增强因子对缺血再灌注损伤肾脏局部炎性反应的影响
- Author:
Xiaohui LIAO
;
Hang SUN
;
Qi LIU
;
Hui GUO
;
Ling ZHANG
- Publication Type:Journal Article
- Keywords:
Reperfusion injury;
Inflammation;
Kidney insufficiency,acute;
Augmenter of liver regeneration
- From:
Chinese Journal of Nephrology
2012;28(2):121-126
- CountryChina
- Language:Chinese
-
Abstract:
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.
