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The Protective Effects of Perindopril Against Acute Kidney Damage Caused by Septic Shock

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Abstract

Acute kidney injury (AKI) resulting from septic shock caused by sepsis is an important health problem encountered at rates of 55–73%. Increasing oxidative stress and inflammation following sepsis is a widely observed condition with rising mortality rates. The purpose of this study was to determine whether perindopril (PER) can prevent sepsis-associated AKI with its antioxidant, anti-inflammatory, and anti-apoptotic effects. The control group received an oral saline solution only for 4 days. Cecal ligation and puncture (CLP)–induced sepsis only was applied to the CLP group, while the CLP + PER (2 mg/kg) received CLP-induced sepsis together with 2 mg/kg PER via the oral route for 4 days before induction of sepsis. Finally, all rats were euthanized by anesthesia and sacrificed. TBARS, total SH levels and NF-κβ, TNF-α, and Caspase-3 expression were then calculated for statistical analysis. TBARS, total SH, NF-kβ/p65, TNF-a, and Caspase-3 levels increased in the CLP group. In contrast, oral administration of PER (2 mg/kg) to septic rats reduced TBARS levels and NF-kβ/p65, TNF-α, and Caspase-3 immunopositivity at biochemical analysis. PER treatment appears to be a promising method for preventing sepsis-induced acute kidney injury through its antioxidant anti-inflammation and anti-apoptotic activities.

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UK, TM, and SB conceived and designed the research. UK and LT conducted the experiments. HKY, HAU, and TM contributed new reagents or analytical tools. UK, HAU, HKY, TM, and SB analyzed the data. UK and TM wrote the manuscript. All authors read and approved the final text.

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Correspondence to Ugur Kostakoglu.

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The authors declare that they have no conflict of interest.

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The study protocol was approved by the Recep Tayyip Erdogan University animal care committee (approval number. 2020/05 dated 28.02.2020).

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Kostakoglu, U., Mercantepe, T., Yilmaz, H.K. et al. The Protective Effects of Perindopril Against Acute Kidney Damage Caused by Septic Shock. Inflammation 44, 148–159 (2021). https://doi.org/10.1007/s10753-020-01316-8

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