Abstract
Renal ischemia/reperfusion (I/R) injury continues to be a complicated situation in clinical practice. Genistein, the main isoflavone found in soy products, is known to possess a wide spectrum of biochemical and pharmacological activities. However, the protective effect of genistein on renal I/R injury has not been well investigated. In the current study, we explore whether genistein exhibits its renal-protective effects through SIRT1 (Sirtuin 1) in I/R-induced mice model. We found the treatment of genistein significantly reduced renal I/R-induced cell death, simultaneously stimulating renal cell proliferation. Meanwhile, SIRT1 expression was up-regulated following the administration of genistein in renal region. Furthermore, pharmacological inhibition or shRNA-mediated depletion of SIRT1 significantly reversed the protective effect of genistein on renal dysfunction, cellular damage, apoptosis, and proliferation following I/R injury, suggesting an indispensible role of the increased SIRT1 expression and activity in this process. Meanwhile, the reduced p53 and p21 expression and increased PCNA (Proliferating Cell Nuclear Antigen) expression were blocked after the depletion of SIRT1 compared with the genistein treatment group in the renal I/R process. Hence, our results provided further experimental basis for the potential use of genistein for the treatment of kidney disease with deficiency of SIRT1 activity.
Highlights
Renal I/R injury is a major cause of acute kidney injury (AKI), which is a clinical condition of frequent occurrence and high mortality [1,2]
The results showed that pre-treatment with 15 mg/kg genistein significantly increased SIRT1 expression in the renal cortex and outer medulla with 15 mg/kg genistein significantly increased SIRT1 expression in the renal cortex and outer compared that inwith the I/R
Renal ischemia-reperfusion is a common cause of acute kidney injury (AKI), which is a common clinical complication characterized by an abrupt decrease in the glomerular filtration rate
Summary
Renal I/R injury is a major cause of acute kidney injury (AKI), which is a clinical condition of frequent occurrence and high mortality [1,2]. I/R injury can increasingly develop into AKI in many clinical settings, such as kidney transplantation, renal artery angioplasty, sepsis, and partial nephrectomy, or by the action of vasoconstrictor drugs and certain hypotensive states [3]. Various pharmaceuticals have been identified for the treatment of renal I/R injury in the laboratory, such as AICAR (5-amino-4-imidazolecarboxamide riboside-1-b-D-ribofuranoside), yohimbine, and pioglitazone [4,5,6]. These are limited, and few renal protectants have been successfully translated into clinical applications. It is critical and urgent to develop safe and effective drugs for treating
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