Augmenter of liver regeneration attenuates inflammation of renal ischemia/reperfusion injury through the NF-kappa B pathway in rats
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  • 作者:Ruyu Yan ; Ying Li ; Ling Zhang ; Ning Xia ; Qi Liu…
  • 关键词:Acute kidney injury ; Ischemia reperfusion injury ; Augmenter of liver regeneration ; Inflammation
  • 刊名:International Urology and Nephrology
  • 出版年:2015
  • 出版时间:May 2015
  • 年:2015
  • 卷:47
  • 期:5
  • 页码:861-868
  • 全文大小:2,320 KB
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  • 作者单位:Ruyu Yan (1)
    Ying Li (1)
    Ling Zhang (1)
    Ning Xia (1)
    Qi Liu (2)
    Hang Sun (2)
    Hui Guo (2)

    1. Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China
    2. Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400010, China
  • 刊物类别:Medicine
  • 刊物主题:Medicine & Public Health
    Nephrology
    Urology and Andrology
  • 出版者:Springer Netherlands
  • ISSN:1573-2584
文摘
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.

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