SGLT2 inhibitor empagliflozin monotherapy alleviates renal oxidative stress in albino Wistar diabetic rats after myocardial infarction induction
| Autor: | Mona A. Abdel‑Kareem, Rasha A. Elsisy, Ahmed S. Ahmed, Marwa M. Mona |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Urology Empagliflozin Infarction RM1-950 Kidney Diabetes Mellitus Experimental 03 medical and health sciences chemistry.chemical_compound Electrocardiography 0302 clinical medicine AKI Glucosides Lipocalin-2 medicine Animals Diabetic Nephropathies Myocardial infarction RNA Messenger Benzhydryl Compounds Rats Wistar Renal Sodium-Glucose Transporter 2 Inhibitors Subclinical infection Pharmacology Creatinine business.industry Acute kidney injury SGLT2 inhibitor General Medicine Acute Kidney Injury medicine.disease Rats Oxidative Stress 030104 developmental biology Elevated serum creatinine medicine.anatomical_structure chemistry 030220 oncology & carcinogenesis Therapeutics. Pharmacology business Cell Adhesion Molecules |
| Zdroj: | Biomedicine & Pharmacotherapy, Vol 139, Iss, Pp 111624-(2021) |
| ISSN: | 0753-3322 |
| Popis: | Acute kidney injury (AKI) is a sudden insult of the kidney that happens within a short period of time, which is associated with poor prognosis in diabetic patients with myocardial infarction (MI). Subclinical AKI is a condition in which tubular damage biomarkers [Neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1(KIM-1)] are positive even in the absence of elevated serum creatinine. Recent studies reported that SGLT-2 inhibitors could protect against subclinical AKI in diabetic patients by elevating the level of β-Hydroxybutyric acid (βOHB). This study aims to examine the reno-protective potential of empagliflozin (EMPA) against MI associated AKI in diabetic rats. Eighty Albino Wistar rats were divided into: (1) nondiabetic sham group (CS), (2) nondiabetic + myocardial infarction group (CM), (3) diabetic + myocardial infarction group (DM) and (4) diabetic + myocardial infarction + empagliflozin group (DME). At the end of the experiment, blood samples and kidneys were collected for biochemical analysis, histopathological, and immunohistochemical studies. After induction of myocardial infarction, there was a significant decrease in serum creatinine and NGAL levels in DME. After EMPA administration, mesangial matrix index and glomerular area were lowered in DME if compared to DM group. As a marker for tubular injury, we used anti-NGAL and anti-KIM-1 immunohistochemistry. Strong positive reaction was noticed in DM group if compared to DME group which showed weak positive reaction. Levels of renal mRNAs [NGAL; KIM-1; Nox-2,4; TLR-2,4; MyD88; TNF- α and IL-1 β, 18] in DME group were reduced significantly compared to DM group. In conclusion, empagliflozin can protect against subclinical acute kidney injury in diabetic albino Wistar rats after myocardial infarction induction, which could improve the clinical outcome of SGLT-2 inhibitors in diabetic patients. |
| Databáze: | OpenAIRE |
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