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.

scholarly journals Cordycepin protects renal ischemia/reperfusion injury through regulating inflammation, apoptosis, and oxidative stress

2020 ◽  
Vol 52 (2) ◽  
pp. 125-132
Author(s):  
Feng Han ◽  
Meng Dou ◽  
Yuxiang Wang ◽  
Cuixiang Xu ◽  
Yang Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Well Being ◽  
Renal Ischemia ◽  
Cordyceps Sinensis ◽  
Renal Ischemia Reperfusion Injury ◽  
And Oxidative Stress

Abstract Cordycepin (3′-deoxyadenosine) is a naturally occurring adenosine analog and one of the bioactive constituents isolated from Cordyceps sinensis, species of the fungal genus Cordyceps. It has traditionally been a prized Chinese folk medicine for the human well-being. However, the actions of cordycepin against renal ischemia/reperfusion injury (I/R) are still unknown. In the present study, rats were subject to I/R and cordycepin was intragastrically administered for seven consecutive days before surgery to investigate the effects and mechanisms of cordycepin against renal I/R injury. The test results of kidney and peripheral blood samples of experimental animals showed that cordycepin significantly decreased serum blood urea nitrogen and creatinine levels and markedly attenuated cell injury. Mechanistic studies showed that cordycepin significantly regulated inflammation, apoptosis, and oxidative stress. These data provide new insights for investigating the natural product with the nephroprotective effect against I/R, which should be developed as a new therapeutic agent for the treatment of I/R in the future.

Study on the Protective Effect of Sevoflurane on H2O2-Induced HK-2 Cells

2019 ◽  
Vol 9 (5) ◽  
pp. 687-693 ◽  
Author(s):  
Cheng Guo ◽  
Jinyue Zhu ◽  
Shuang Wu ◽  
Xia Li ◽  
Ying Ding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Control Group ◽  
Renal Ischemia Reperfusion Injury ◽  
And Oxidative Stress

Background: Renal ischemia reperfusion injury (RIRI) is the main cause of acute kidney injury (AKI). The aim of this study was to investigate whether sevoflurane could protect HK-2 cells treated by H2O2 by improving apoptosis and oxidative stress through TLR4/MyD88/NF-κb signaling pathway. Methods: HK-2 cells was treated with H2O2 to construct the oxidative damage model happened in renal ischemia reperfusion injury (RIRI). CCK-8 assay was performed to analyze the viability of HK-2 cells. The reactive oxygen species (ROS), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdelyde (MDA) testing kits were used for the detection of oxidative stress related factors. TUNEL assay and Western blot were applied to analyze the apoptosis of HK-2 cells. And, proteins of TLR4/MyD88/NF-κb signaling pathway were also detected by western blot. Results: The viability of H2O2-induced HK-2 cells was decreased compared with the control group. The ROS, SOD and MDA levels were increased and LDH level was decreased in H2O2-induced HK-2 cells. The apoptosis of H2O2-induced HK-2 cells was increased. The expression of Bax was decreased and the expression of Bcl-2 and cleaved caspase 3 were increased in the H2O2-induced HK-2 cells. The expression of TLR4/MyD88/NF-κb signaling pathway was increased in the H2O2-induced HK-2 cells. All these changes were reversed by pretreatment with sevoflurane to some extent in HK-2 cells. Conclusion: In conclusion, sevoflurane pretreatment protects HK-2 cells treated by H2O2 by improving apoptosis and oxidative stress through inhibiting the TLR4/MyD88/NF-κb signaling pathway.

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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