Augmenter of liver regeneration attenuates inflammation of renal ischemia/reperfusion injury through the NF-kappa B pathway in rats

Int Urol Nephrol. 2015 May;47(5):861-8. doi: 10.1007/s11255-015-0954-8. Epub 2015 Mar 20.

Abstract

Purpose: 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.

Conclusion: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / etiology
  • Acute Kidney Injury / metabolism
  • Acute Kidney Injury / pathology
  • Acute Kidney Injury / prevention & control*
  • Animals
  • Apoptosis / drug effects
  • Blood Urea Nitrogen
  • CD11b Antigen / analysis
  • Cell Count
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Creatinine / blood
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Kidney Tubules / chemistry*
  • Kidney Tubules / pathology*
  • Kidney Tubules / physiopathology
  • Male
  • Necrosis / prevention & control
  • Nephritis / etiology
  • Nephritis / metabolism
  • Nephritis / prevention & control*
  • Neutrophils / chemistry
  • Proteins / therapeutic use*
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / complications
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Reperfusion Injury / prevention & control*
  • Signal Transduction / drug effects*
  • Transcription Factor RelA / genetics
  • Transcription Factor RelA / metabolism*

Substances

  • CD11b Antigen
  • Ccl2 protein, rat
  • Chemokine CCL2
  • Interleukin-1beta
  • Interleukin-6
  • Proteins
  • RNA, Messenger
  • Transcription Factor RelA
  • GFER protein, rat
  • Creatinine