Prophylactic effect of ethyl pyruvate on renal ischemia/reperfusion injury mediated through oxidative stress

2018 ◽  
Vol 51 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Jonathan Bloom ◽  
Neel Patel ◽  
Jonathan Wagmaister ◽  
Muhammad Choudhury ◽  
Majid Eshghi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ethyl Pyruvate ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Prophylactic Effect ◽  
Renal Ischemia Reperfusion Injury

scholarly journals Prophylactic effect of ethyl pyruvate on renal ischemia/reperfusion injury in rats

2021 ◽  
Vol 8 (4) ◽  
pp. 102-107
Author(s):  
Roger Yau ◽  
Jonathan Bloom ◽  
Jonathan Wagmaister ◽  
Majid Eshghi ◽  
Muhammad Choudhury ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ethyl Pyruvate ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Primary Role ◽  
Renal Ischemia Reperfusion Injury ◽  
And Oxidative Stress

Background: Following our hypothesis that oxidative stress might play a primary role in renal ischemia/reperfusion injury (RIRI), we investigated if ethyl pyruvate (EPy) with potent antioxidant activity might prevent or alleviate RIRI induced in rats. Methods: Sprague-Dawley rats were randomly divided into four groups: (A) Sham, (B) renal ischemia/reperfusion (RIR), (C) RIR with EPy supplement (RIR+EPy), and (D) RIR with Mann supplement (RIR+Mann). Mannitol (Mann), a preoperative agent being clinically used, was tested for comparison with EPy. Rats were subjected to 40-min ischemia, followed by 24-h reperfusion. Either EPy or Mann was given to rats 30 min prior to ischemia and immediately before the reperfusion period. Results: The RIR and RIR+Mann groups showed palpable kidney injuries with the ~5-fold elevated blood urea nitrogen (BUN) and creatinine (Cr) levels, indicating renal dysfunction. However, the kidneys in the RIR+EPy group appeared merely normal (similar to the Sham’s) with the basal BUN/Cr levels, indicating normal renal function. No effects on histology, BUN or Cr were yet seen with Mann. Moreover, specific kidney injury markers were up-regulated and oxidative stress was also ~2.1-fold severer in the RIR group, whereas little changes in those markers and oxidative stress were seen with EPy supplement (RIR+EPy). Conclusions: Although oxidative stress feasibly plays a key role in RIRI, EPy with antioxidant activity is capable of protecting the kidneys from such an assault. Thus, EPy (not Mann) should be considered as an effective perioperative renoprotective agent that could be used clinically.

Effects of Kallistatin on Oxidative Stress and Inflammation on Renal Ischemia-Reperfusion Injury in Mice

2015 ◽  
Vol 13 (2) ◽  
pp. 265-273 ◽  
Author(s):  
Shuqin Zhou ◽  
Yingying Sun ◽  
Yugang Zhuang ◽  
Wei Zhao ◽  
Yuanzhuo Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

Hydrogen Sulfide Reduces Renal Ischemia-Reperfusion Injury by Enhancing Autophagy and Reducing Oxidative Stress

2021 ◽  
Author(s):  
Hui Li ◽  
Shuaiwei Wang ◽  
Shuangshuang An ◽  
Biao Gao ◽  
Tieshan Teng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Beclin 1 ◽  
Dependent Manner ◽  
Protein Levels ◽  
Renal Ischemia Reperfusion Injury

Abstract Background Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury. Hydrogen sulfide (H2S) exerts a protective effect in renal IRI. The present study was carried out to investigate the effects of exogenous H2S on renal IRI by regulating autophagy in mice. Methods Mice were randomly assigned to control, IRI, and NaHS (28, 56 and 100 µmol/kg) groups. Renal IRI was induced by clamping the bilateral renal pedicles for with non-traumatic arterial clamp for 45 min and then reperfused for 24 h. Mice were administered intraperitoneally with NaHS 20 min prior to renal ischemia. Sham group mice underwent the same procedures without clamping. Serum and kidney tissues were harvested 24 h after reperfusion for functional, histological, oxidative stress, and autophagic determination. Results Compared with the control group, the concentrations of serum creatinine (Scr), blood urea nitrogen (BUN), and malondialdehyde (MDA), the protein levels of LC3II/I, Beclin-1, and P62, as well as the number of autophagosomes were significantly increased, but the activity of superoxide dismutase (SOD) was decreased after renal IRI. NaHS pretreatment dramatically attenuated renal IRI-induced renal dysfunction, histological changes, MDA concentration, and p62 expression in a dose-dependent manner. However, NaHS increased the SOD activity and the protein levels of LC3II/I and Beclin-1. Conclusions These results indicate that exogenous H2S protects the kidney from IRI through enhancement of autophagy and reduction of oxidative stress. Novel H2S donors could be developed in the treatment of renal IRI.

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