title: Augmenter of liver regeneration attenuates inflammation of renal ischemia/reperfusion injury through the NF-kappa B pathway in rats.
abstract: OBJECTIVE
  The effects of augmenter of liver regeneration (ALR) on the acute kidney injury (AKI) rats were investigated by measuring the inflammatory response associated with transcription factor nuclear factory (NF-κB) pathway.
  
  
  METHODS
  The model of AKI rats was established by occluded the renal pedicles for 60 min and then released. After that, animals were treated with ALR (100 or 200 μg/kg). All rats were killed at different time points (24, 48, 72 h). Renal function and kidney histological changes were measured. The apoptosis of tubular cells was evaluated by TdT-mediated dUTP nick end labeling assay. Cytokines and chemokines were assessed by immunohistochemistry, enzyme-linked immunosorbent assay and real-time polymerase chain reaction (RT-PCR). The NF-κB p65 protein was analyzed by immunohistochemistry and RT-PCR, respectively.
  
  
  RESULTS
  Ischemia reperfusion induced tubular cells necrosis and apoptosis, and ALR can significantly reduce this damages. The productions of MCP-1, IL-1β and IL-6 were lower in the group of ALR treatment, especially in the high-dose group. The inflammatory infiltrates were lower in the rats with administration of ALR. ALR mediated the level of cytokines and chemokines through inhibited the activation of NF-κB.
  
  
  CONCLUSIONS
  ALR can improve renal function and inhibit the expression of inflammatory factors. This protects against renal ischemia reperfusion injury, which may be associated with preventing NF-κB activation in rats.
authors: Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China, yrysuperman@126.com.
authors: Ruyu
authors: R
authors: Yan
authors: Ying
authors: Y
authors: Li
authors: Ling
authors: L
authors: Zhang
authors: Ning
authors: N
authors: Xia
authors: Qi
authors: Q
authors: Liu
authors: Hang
authors: H
authors: Sun
authors: Hui
authors: H
authors: Guo
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001806:Blood Urea Nitrogen; D039481:CD11b Antigen / Q000032:analysis; D002452:Cell Count; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007684:Kidney Tubules / Q000737:chemistry* / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009336:Necrosis / Q000517:prevention & control; D009393:Nephritis / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D009504:Neutrophils / Q000737:chemistry; D011506:Proteins / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D015398:Signal Transduction / Q000187:drug effects*; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism*; D050862:Oxidoreductases Acting on Sulfur Group Donors
chemical_list: D039481:CD11b Antigen; D018932:Chemokine CCL2; D003404:Creatinine; D053583:Interleukin-1beta; D015850:Interleukin-6; D011506:Proteins; D012333:RNA, Messenger; D051996:Transcription Factor RelA; C491766:Ccl2 protein, rat; C088825:GFER protein, rat; D050862:Oxidoreductases Acting on Sulfur Group Donors