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The protective effect of Edaravone against acute renocardiac syndrome in a kidney ischemia-reperfusion model
Yasin Bagheri1, Mahshid Dehghan2, Seyyedeh Mina Hejazian1
1Kidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Introduction:
Acute kidney injury (AKI) is a common clinical occurrence causing high mortality and morbidity. In acute renocardiac syndrome, AKI leads to acute cardiac injury or/and dysfunction. This study aimed to investigate the antioxidative effects of Edaravone on cardiac tissues following the induction of renal ischemia-reperfusion injury (IRI) in rats.
Methods:
Twenty-four male Wistar rats were randomly divided into four groups: IR+Edaravone, Edaravone, IR, and Sham groups (six rats per group). Non-traumatic clamps were used to stop the artery and vein blood flow of the left kidney in rats of the IR groups for 45 minutes. Thirty minutes before ischemia induction, Edaravone (3 mg/kg) was injected intraperitoneally in the IR+Edaravone group. Cardiac samples were subjected to biochemical analyses.
Results:
The Results showed a significant increase in the enzymatic activity of glutathione peroxidase (P=0.01), catalase (P=0.03), and superoxide dismutase (P=0.02), and the levels of glutathione (P=0.012), and total antioxidant capacity (P<0.001) in the IR+Edaravone group in comparison to the IR group. Moreover, the total antioxidant capacity of the heart was increased in the Edaravone group compared to the control and IR groups (P<0.001), indicating the safety of the drug.
Conclusion:
The results can reveal important insights into the protective effects of Edaravone against acute renocardiac syndrome.
Insights
Edaravone treatment significantly boosted antioxidant enzymes and capacity in rat cardiac tissues after kidney injury. This suggests Edaravone offers protective benefits against acute renocardiac syndrome.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Pharmacology
Background:
- Acute kidney injury (AKI) is a prevalent condition associated with high mortality and morbidity.
- AKI can precipitate acute cardiac injury or dysfunction, a condition known as acute renocardiac syndrome.
- Investigating protective strategies against renocardiac syndrome is crucial for improving patient outcomes.
Purpose of the Study:
- To evaluate the antioxidative effects of Edaravone on cardiac tissues following renal ischemia-reperfusion injury (IRI) in a rat model.
- To determine if Edaravone can mitigate cardiac damage associated with AKI-induced renocardiac syndrome.
Main Methods:
- Male Wistar rats were divided into four groups: IR+Edaravone, Edaravone, IR, and Sham.
- Renal ischemia-reperfusion injury was induced by clamping the left kidney for 45 minutes.
- Edaravone (3 mg/kg) was administered intraperitoneally 30 minutes before ischemia induction in the IR+Edaravone group.
- Cardiac tissues were collected for biochemical analysis of antioxidant markers.
Main Results:
- Edaravone treatment significantly increased the enzymatic activity of glutathione peroxidase, catalase, and superoxide dismutase in cardiac tissues compared to the IR group.
- Levels of glutathione and total antioxidant capacity in the heart were significantly elevated in the IR+Edaravone group.
- Edaravone administration alone also increased cardiac total antioxidant capacity, indicating its safety.
Conclusions:
- Edaravone demonstrates significant antioxidative effects in cardiac tissues following renal IRI.
- These findings suggest Edaravone has protective potential against acute renocardiac syndrome.
- Further research into Edaravone's role in managing renocardiac complications is warranted.
