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

Jelena Nesovic Ostojic,Nevena Mihailovic-Stanojevic,Danijela Karanovic,Senka Ljubojevic-Holzer,Zoran Miloradovic,Milan Ivanov,Predrag Brkic,Sanjin Kovacevic,Rada Jeremic,Maja Zivotic,Djurdjica Jovovic,Una Jovana Vajic

doi:10.3390/ijms22031382

Jelena Nesovic Ostojic, Nevena Mihailovic-Stanojevic + Show 10 more

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https://doi.org/10.3390/ijms22031382

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Abstract

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.

Highlights

Acute kidney injury (AKI) is manifested by a rapid decline in renal function, especially glomerular filtration rate (GFR), occurring over a few hours or days, followed by failure to maintain fluid, electrolyte and acid-base homeostasis [1]
Both in normotensive and hypertensive groups Systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) were significantly decreased in AKI group compared to SHAM group
We demonstrated significant improvement of GFR in AKI + hyperbaric oxygen (HBO) compared to AKI group in rats with and without hypertension

Summary

Introduction

Acute kidney injury (AKI) is manifested by a rapid decline in renal function, especially glomerular filtration rate (GFR), occurring over a few hours or days, followed by failure to maintain fluid, electrolyte and acid-base homeostasis [1]. Hypertension and older age are risk factors for acute kidney injury [2]. AKI is recognized as a potential in-hospital complication of sepsis, heart condition and surgery [2,3]. Renal ischemia and reperfusion (I/R) injury is the most common cause of AKI [4]. Pathogenesis of renal I/R injury involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis [4]. The relative contribution of each to decline GFR is uncertain [5]. Therapeutic approaches to treat AKI are extremely limited, so all efforts are made to prevention, early detection of the disorder and establishing secondary preventive measures to impede AKI progression [6]

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