Protective effects of lupeol in rats with renal ischemia‑reperfusion injury

• Published in: Experimental and therapeutic medicine 2024-08, Vol.28 (2), Article 313
• Main Authors: Kapisiz, Alparslan, Kaya, Cem, Eryilmaz, Sibel, Karabulut, Ramazan, Turkyilmaz, Zafer, Inan, Mehmet Arda, Gulbahar, Ozlem, Sonmez, Kaan
• Format: Article
• Language: English
• Subjects: Abdomen; Acute renal failure; Analysis; Animals; Antioxidants; Apoptosis; Cancer therapies; Care and treatment; Complications and side effects; Creatinine; Diagnosis; Health aspects; Ischemia; Ketamine; Kidney function tests; Kidneys; Kinases; Laparotomy; Risk factors; Toxicity; Veins & arteries
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2024.12602

Acute kidney injury (AKI) caused by ischemia and, exogenous or endogenous nephrotoxic agents poses a serious health issue. AKI is seen in 1% of all hospital admissions, 2-5% of hospitalizations and 67% of intensive care unit (ICE) patients. The in-hospital mortality rates for AKI is 40-50, and >50% for ICE patients. Ischemia-reperfusion (I/R) injury in the kidney can activate inflammatory responses and oxidative stress, resulting in AKI. The common endpoint in acute tubular necrosis is a cellular insult secondary to ischemia or direct toxins, which results in effacement of brush border, cell death and decreased function of tubular cells. The aim of the present study was to assess if the reported antioxidant and anti-inflammatory agent lupeol can exert any effects against renal I/R damage. In total, 24 Wistar Albino rats were randomly assigned into four groups of 6, namely Sham, lupeol, ischemia and therapy groups. In the lupeol group, intraperitoneal administration of 100 mg/kg lupeol was given 1 h before laparotomy, whilst only laparotomy was conducted in the sham group. The renal arteries of both kidneys were clamped for 45 min, 1 h after either intraperitoneal saline injection (in the ischemia group) or 100 mg/kg lupeol application (in the therapy group). The blood samples and renal tissues of all rats were collected after 24 h. In blood samples, blood urea nitrogen (BUN) was measured by the urease enzymatic method, and creatinine was measured by the kinetic Jaffe method. Using ELISA method, TNF-[alpha] and IL-6 levels were measured in the blood samples, whereas malondialdehyde (MDA), glutathione (GSH), caspase-3 levels were measured in kidney tissues. In addition, kidney histopathological analysis was performed by evaluating the degree of degeneration, tubular dilatation, interstitial lymphocyte infiltration, protein cylinders, necrosis and loss of brush borders. It was determined that renal damage occurred due to higher BUN, creatinine, MDA, TNF-[alpha] and caspase-3 values observed in the kidney tissues and blood samples of rats in ischemia group compared with the Sham group. Compared with those in the ischemia group, rats in the therapy group exhibited increased levels of GSH and reduced levels of BUN, TNF-[alpha], MDA. Furthermore, the ischemia group also had reduced histopathological damage scores. Although differences in creatinine, IL-6 and caspase-3 levels were not statistically significant, they were markedly reduced in the treatment group. Ta