Protective effect of epigallocatechin gallate, a major constituent of green tea, against renal ischemia–reperfusion injury in rats
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  • 作者:Jun Lv ; Min Feng ; LiLi Zhang ; Xia Wan ; Yu Chun Zeng…
  • 关键词:EGCG ; Inflammation ; Apoptosis ; Renal ischemia–reperfusion injury
  • 刊名:International Urology and Nephrology
  • 出版年:2015
  • 出版时间:August 2015
  • 年:2015
  • 卷:47
  • 期:8
  • 页码:1429-1435
  • 全文大小:3,440 KB
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  • 作者单位:Jun Lv (1)
    Min Feng (1)
    LiLi Zhang (1)
    Xia Wan (1)
    Yu Chun Zeng (1)
    Pei Fen Liang (1)
    An Ping Xu (1)

    1. Department of Nephrology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, People’s Republic of 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
Background Renal ischemia–reperfusion (I/R) injury plays an important role in the acute kidney injury. The pathogenetic mechanisms potential I/R?injury is involved in apoptosis and inflammation. Epigallocatechin gallate (EGCG), a major constituent of green tea, has been shown to have anti-inflammatory and anti-apoptotic activities. This study aimed to explore the underlying effects and mechanisms of EGCG on renal I/R injury in a rat model. Materials and methods We induced renal I/R injury in SD rats by clamping the left renal artery for 45?min followed by 24-h reperfusion, along with a contralateral nephrectomy. We randomly allocated 30 rats to three groups (n?=?10): sham group, IRI group, and EGCG group. We preconditioned rats intraperitoneally with EGCG (50?mg/kg) or vehicle (50?mg/kg) 45?min before inducing renal ischemia. We collected serum and kidneys at 24?h after reperfusion. Renal function and histologic damage were assessed. We also determined markers of inflammation and apoptosis in kidneys or serum. Results EGCG pretreatment can significantly reduce renal dysfunction, histologic change and the expression of tumor necrosis factor-α, IL-1β, IL-6, Bax and cleavage caspase 3 induced by I/R injury and increase the expression of Bax and caspase 3. Moreover, EGCG pretreatment can further induce the activation of p38 mitogen-activated protein kinase in kidney, with no influence on the expression of p38. Conclusions EGCG treatment can decrease renal ischemia–reperfusion injury by suppressing inflammation and cell apoptosis. Thus, EGCG may represent a potential strategy to reduce renal I/R injury.
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