Abstract
Introduction The acute kidney injury (AKI) is characterized by a sudden glomerular filtration reduction. Renal or intrinsic causes of AKI include nephrotoxicity induced by exogenous agents like cisplatin, which causes oxidative stress altering the biochemical process and leading to apoptosis. Therefore, this research is aimed at analyzing the embryonic stem cells (ESC) nephroprotective effect in AKI induced by cisplatin, employing genetic, phenotypic, and microspectroscopic techniques. Methods Thirty mice were randomly divided into three groups (n = 10): the healthy, isotonic salt solution (ISS), and mouse embryonic stem cells (mESC) groups. The ISS and mESC groups were subjected to AKI using cisplatin; 24 h post-AKI received an intraperitoneal injection of ISS or 1 × 106 mESC, respectively. At days 4 and 8 post-AKI, five mice of each group were sacrificed to analyze the histopathological, genetic (PDK4 and HO-1), protein (p53), and vibrational microspectroscopic changes. Results Histopathologically, interstitial nephritis and acute tubular necrosis were observed; however, the mESC group showed a more preserved microarchitecture with high cellularity. Additionally, the PDK4 and HO-1 gene expression only increased in the ISS group on day 4 post-AKI. Likewise, p53 was more immunoexpressed at day 8 post-AKI in the ISS group. About biomolecular analysis by microspectroscopy, bands associated with lipids, proteins, and nucleic acids were evidenced. Besides, ratios related to membrane function (protein/lipid), unsaturated lipid content (olefinic/total lipid, olefinic/total CH2, and CH2/CH3), and lipid peroxidation demonstrated oxidative stress induction and lipid peroxidation increase mainly in the ISS group. Finally, the principal component analysis discriminated against each group; nonetheless, some data of the healthy and mESC groups at day 8 were correlated. Conclusions The mESC implant diminishes cisplatin nephrotoxicity, once the protective effect in the reduction of lipid peroxidation was demonstrated, reflecting a functional and histological restoration.
Highlights
The acute kidney injury (AKI) is characterized by a sudden glomerular filtration reduction
Renal function was checked through creatinine serum levels 48 h prior AKI in the isotonic salt solution (ISS) and mouse embryonic stem cells (mESC) groups, which exhibited normal values (0 69 ± 0 19 for the ISS group and 0 73 ± 0 17 mg/dl for the mESC group)
This metabolite was evaluated at day 8 post-AKI evidencing a decrement (1 62 ± 0 83 for the ISS group and 1 15 ± 0 11 mg/dl for the mESC group) (Figure 1)
Summary
The acute kidney injury (AKI) is characterized by a sudden glomerular filtration reduction. Renal or intrinsic causes of AKI include nephrotoxicity induced by exogenous agents like cisplatin, which causes oxidative stress altering the biochemical process and leading to apoptosis. The therapies for AKI involve the use of continuous renal replacement techniques indicated for fluid management, correction of electrolyte and pH problems, and treatments for clinical alterations secondary to uremia [2], but these therapies do not resolve the progressive decrease of renal function. These techniques represent the primary treatment against kidney injury (KI), they are associated with high morbidity and mortality. It is necessary to explore new alternative therapies for nephropathic patients, seeking a definitive treatment for KI, which might increase tissue regeneration and renal function [3]
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