scholarly journals Immunohistochemical Analysis of 4-HNE, NGAL, and HO-1 Tissue Expression after Apocynin Treatment and HBO Preconditioning in Postischemic Acute Kidney Injury Induced in Spontaneously Hypertensive Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1163
Author(s):  
Sanjin Kovacevic ◽  
Milan Ivanov ◽  
Maja Zivotic ◽  
Predrag Brkic ◽  
Zoran Miloradovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Spontaneously Hypertensive Rats ◽  
Kidney Injury ◽  
Immunohistochemical Analysis ◽  
Tissue Expression ◽  
Pure Oxygen ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Renal Expression

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.

scholarly journals Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

2021 ◽  
Vol 22 (3) ◽  
pp. 1382
Author(s):  
Jelena Nesovic Ostojic ◽  
Milan Ivanov ◽  
Nevena Mihailovic-Stanojevic ◽  
Danijela Karanovic ◽  
Sanjin Kovacevic ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protein Expression ◽  
Hyperbaric Oxygen ◽  
Heme Oxygenase ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Kidney Injury ◽  
Heme Oxygenase 1 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.

P0551THE EFFECTS OF HYPERBARIC OXYGEN PRECONDITIONING AND APOCYNIN TREATMENT IN POSTISCHEMIC ACUTE KIDNEY INJURY INDUCED IN SPONTANEOUSLY HYPERTENSIVE RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sanjin Kovacevic ◽  
Milan Ivanov ◽  
Zoran Miloradovic ◽  
Predrag Brkic ◽  
Una-Jovana Vajic ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Mortality Rates ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tubular Necrosis ◽  
Renal Ischemia Reperfusion Injury

Abstract Background and Aims Acute kidney injury (AKI) is associated with significant in-hospital morbidity and mortality, particularly in those admitted to the Intensive care units, where mortality rates may exceed 50%. Besides increased mortality rates, there are chronic consequences that carry high risk of developing or exacerbating chronic kidney disease and accelerated development of the end-stage renal disease. Renal ischemia/reperfusion injury is a common cause of AKI and hypertension might contribute to the increased incidence of AKI. The purpose of this study was to investigate the effects of combined hyperbaric oxygen (HBO) preconditioning and apocynin treatment on kidney hemodynamics, function and structure in spontaneously hypertensive rats (SHR) after renal ischemia reperfusion injury. Method Male SHR were randomly selected in three experimental groups: sham-operated group (SHAM, n=9), AKI control group (AKI, n=11) and AKI group with HBO preconditioning and apocynin treatment (AKI+APO+HBO, n=13). HBO preconditioning was performed by exposing to pure oxygen (2.026 bar) twice a day for two consecutive days for 60 minutes and day before AKI induction. All surgical procedures were performed in anaesthetized rats and AKI was induced by removal of the right kidney and atraumatic clamp occlusion of the left renal artery for 45 minutes. NADPH oxidase inhibitor, apocynin (40 mg/kg b.m., intravenously) was applied as a bolus injection 5 minutes before clamp removal. All hemodynamic parameters were measured 24 hours after reperfusion. After hemodynamic measurements, blood samples were collected and used for further analysis. Animals were sacrificed by pentobarbital overdose injection. Kidney tissue was removed and then prepared for histological examination. Results AKI significantly increased renal vascular resistance (RVR, p<0.001) and reduced renal blood flow (RBF, p<0.001), which were significantly improved in group with HBO preconditioning with apocynin treatment (RVR, p<0.05; RBF, p<0,01). AKI induction significantly increased plasma creatinine (p<0.001), urea (p<0.001), phosphate (p<0.001) levels. Remarkable improvement, with decrease in creatinine (p<0.001), urea (p<0.01) and phosphate (p<0.001) levels was observed in treated group. While AKI induction significantly increased plasma KIM – 1 levels (p<0.001), HBO preconditioning with apocynin treatment decreased its levels (p<0.05). Considering renal morphology, in SHAM operated rats, normal morphology of glomeruli, tubulointerstitium, and blood vessels were observed including rare kidney specimens with a few PAS positive casts in the lumen of the tubules. In animals with AKI significant morphological alterations were present: tubular cells necrosis, dilatation of certain segments of the proximal and distal tubules, mostly with loss of brush-border. The most notable changes were present in the cortico-medullary zone, where the broad areas of tubular necrosis and a large number of PAS positive casts in the collecting ducts were observed. In treated animals degrees of morphological changes were significantly lower compared to AKI control. There were reduced tubular dilatation, tubular necrosis in the cortico-medullary zone and PAS positive cast formation. Conclusion HBO preconditioning and apocynin treatment improve renal hemodynamics, function and in SHR which suffer AKI. These results suggest that it is reasonable to assume that HBO preconditioning and NADPH oxidase inhibition potentially may have beneficial effects, but further comprehensive experimental and clinical studies are needed to confirm these promising results.

Hyperbaric oxygenation protects the kidney against ischemia-reperfusion injury

2020 ◽  
pp. 21-30
Author(s):  
Milan Ivanov ◽  
◽  
Predrag Brkic ◽  
Una-Jovana Vajic ◽  
Nevena Mihailovic-Stanojevic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Kidney Function ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Hemodynamics ◽  
Pure Oxygen ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Background: Acute kidney injury (AKI) as a consequence of ischemia is a common clinical event that can lead to unacceptably high morbidity and mortality. Hyperbaric oxygen (HBO2) preconditioning has been shown to prevent ischemia-reperfusion injury (IRI) in different tissues. Objectives: The aim of our study was to compare the effects of HBO2 preconditioning on renal hemodynamics, kidney function and oxidative stress in normotensive and spontaneously hypertensive rats that suffered kidney IRI. Methods: An experiment was performed on Wistar (normotensive) and spontaneously hypertensive rats (SHR). The animals were divided into the following experimental groups: sham-operated rats and rats with or without HBO2 preconditioning 24 hours before post-ischemic AKI induction. Treated rats were placed into experimental HBO2 chambers and exposed to pure oxygen twice a day for two consecutive days (2.026 bar of oxygen) for 60 minutes. AKI was performed the next morning. The right kidney was removed and the renal ischemia was performed by clamping the left renal artery for 45 minutes. Results: In this study, HBO2 preconditioning significantly improved disturbed renal hemodynamics, major markers of kidney function in plasma (creatinine, urea and phosphate) as well as antioxidant enzymes (superoxide dismutase and catalase) activities in erythrocytes after AKI induction. Also, HBO2 preconditioning decreased lipid peroxidation in plasma after ischemic AKI. Positive effects were observed in both strains of rats. Conclusions: Our results suggest that HBO2 treatment improves renal hemodynamic and kidney function and decreases oxidative stress of Wistar and SHR rats with an AKI episode. Furthermore, it also implies that pre-existing hypertension does not affect the beneficial effects of HBO2 preconditioning.

In Vivo Evidence for Microvascular Oxidative Stress in Spontaneously Hypertensive Rats

Hypertension ◽  
1995 ◽  
Vol 25 (5) ◽  
pp. 1083-1089 ◽  
Author(s):  
Hidekazu Suzuki ◽  
Allen Swei ◽  
Benjamin W. Zweifach ◽  
Geert W. Schmid-Schönbein
Keyword(s):  
Oxidative Stress ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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