Abstract
Oxidative stress has been considered as a central aggravating factor in the development of postischemic acute kidney injury (AKI). The aim of this study was to perform the immunohistochemical analysis of 4-hydroxynonenal (4-HNE), neutrophil gelatinase-associated lipocalin (NGAL), and heme oxygenase-1 (HO-1) tissue expression after apocynin (APO) treatment and hyperbaric oxygenation (HBO) preconditioning, applied as single or combined protocol, in postischemic acute kidney injury induced in spontaneously hypertensive rats (SHR). Twenty-four hours before AKI induction, HBO preconditioning was carried out by exposing to pure oxygen (2.026 bar) twice a day, for 60 min in two consecutive days. Acute kidney injury was induced by removal of the right kidney while the left renal artery was occluded for 45 min by atraumatic clamp. Apocynin was applied in a dose of 40 mg/kg body weight, intravenously, 5 min before reperfusion. We showed increased 4-HNE renal expression in postischemic AKI compared to Sham-operated (SHAM) group. Apocynin treatment, with or without HBO preconditioning, improved creatinine and phosphate clearances, in postischemic AKI. This improvement in renal function was accompanied with decreased 4-HNE, while HO-1 kidney expression restored close to the control group level. NGAL renal expression was also decreased after apocynin treatment, and HBO preconditioning, with or without APO treatment. Considering our results, we can say that 4-HNE tissue expression can be used as a marker of oxidative stress in postischemic AKI. On the other hand, apocynin treatment and HBO preconditioning reduced oxidative damage, and this protective effect might be expected even in experimental hypertensive condition.
Highlights
The main causes of acute kidney injury are linked to ischemia and hypoxia
We showed for the first time that 4-HNE can be used as a marker of oxidative stress in postischemic acute kidney injury induced in hypertensive rats, and that APO treatment, as well as hyperbaric oxygenation (HBO) preconditioning, decreased the expression of 4-HNE, in kidney tissue
4-HNE can be used as a marker of oxidative stress in postischemic acute kidney injury animal model
Summary
The main causes of acute kidney injury are linked to ischemia and hypoxia. Decreased renal blood flow is followed by reduced nutrient and oxygen uptake, which provokes acute tubular necrosis and induces inflammation [1]. Antioxidants 2021, 10, 1163 of reactive oxygen species (ROS) determines deleterious effects on biomolecules DNA, RNA, proteins, lipids, enzymes, and so on. These changed biomolecules could be detected and used for oxidative stress [4]. Besides ROS, which are inevitable by-products of oxidative stress, there are secondary intermediates such as 4-hydroxynonenal (4-HNE). 4-HNE is a product of lipid peroxidation and may serve as a non-invasive biomarker of oxidative stress [6,7]. In addition to its multiple physiological processes, 4-HNE has been associated with different diseases, such as Alzheimer’s disease, Parkinson’s disease, heart disease, atherosclerosis, cancers, diabetes, and acute lung injury [10,11,12,13,14]
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