Key result
Lisinopril and enalapril reverse doxorubicin-induced acute kidney injury by suppressing oxidative stress and inflammation.
Why the study?
Doxorubicin causes nephrotoxicity limiting its clinical use, and combining it with ACE inhibitors may reduce acute kidney injury.
Does Lisinopril or Enalapril reduce doxorubicin-induced acute kidney injury in male Wistar rats?
Does Lisinopril or Enalapril reduce doxorubicin-induced acute kidney injury in male Wistar rats?
Lisinopril and Enalapril ameliorate doxorubicin-induced acute kidney injury in a rat model by reducing oxidative stress and inflammation.
May attenuate DOX-induced AKI in rats; leaves open whether ACE inhibitors protect kidneys during chemotherapy.
Doxorubicin (DOX) is a standard anticancer agent exerting devastating effects as nephrotoxicity, hepatotoxicity and cardiotoxicity. The purpose of this study was to increase the clinical use of DOX through decreasing its detrimental effects via combination with ACE inhibitors to ameliorate the induced acute kidney injury (AKI). AKI was induced by a single injection of DOX (7.5 mg/kg; i.p.) as Group 1; control (vehicle), Group 2; DOX (7.5 mg/kg; i.p.) single dose, Group 3 and 4; Lisinopril (Lis, 20 mg/kg) and Enalapril (Enal, 40 mg/kg) orally administration for 15 consecutive days after DOX injection, respectively. Serum samples were used to measure creatinine and BUN, tissue samples were extracted to determine myeloperoxidase (MPO), malondialdehyde (MDA), total antioxidant capacity (TAC) and kidney injury molecule (KIM-1) using ELISA technique. Heme oxygenase (HO-1) RNA expression was quantified in tissue using real time polymerase chain reaction (PCR). Parts of the kidney tissue were kept in formalin for immunohistochemical demonstration of Cleaved Caspase-3 and NF-κβ immune staining and the other part was used for pathological examination. Oral treatment with Lis (20 mg/kg) and Enal (40 mg/kg) for 15 consecutive days reversed DOX effects as they reduced the serum creatinine and BUN, kidney levels of MPO and MDA, whereas the drugs increased tissue TAC. The administration of Lis and Enal with DOX also reduced KIM-1and HO-1 RNA expression. A significant decrease in cleaved caspase-3 and NF-κβ immunostainings in conjunction with pronounced amelioration in pathologies in the rat kidney were observed. We concluded that DOX adverse effects can be controlled by Lis and Enal.
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Hassan et al. (2021) studied Doxorubicin-induced acute kidney injury. Lisinopril and Enalapril vs. Doxorubicin alone and vehicle control was evaluated on Serum creatinine, BUN, MPO, MDA, TAC, KIM-1, HO-1 RNA expression, cleaved caspase-3, and NF-κβ. Oral treatment with Lisinopril and Enalapril reversed doxorubicin-induced acute kidney injury in male Wistar rats by reducing serum creatinine, BUN, and markers of oxidative stress and inflammation.
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