Histological study on the protective effect of endogenous stem-cell mobilization in Adriamycin-induced chronic nephropathy in rats

Sadek, Eman Mostafa; Salama, Nagla M.; Ismail, Dalia Ibrahim; El-Shafei, Asmaa

doi:10.1016/j.jmau.2015.12.003

Cited by 12 publications

(9 citation statements)

References 35 publications

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“…Histological finings revealed nearly normal renal architecture. This was confirmed by others [30] . who stated that G-CSF improved mobilization of endogenous hemopoietic stem cells (HSCs), so restored normal renal structure and reduced renal injury and development of reactive oxygen species (ROS) and levels of urea and creatinine.…”

Section: Mobilizationsupporting

confidence: 84%

Impact of Remdesivir on the kidney and potential protective capacity of Granulocyte-Colony Stimulating Factor versus Bone Marrow Mesenchymal Stem Cells in adult male albino rats

El-Haroun

Bashandy

Soliman

2021

Egyptian Journal of Histology

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Background: Remdesivir is a novel broad spectrum antiviral drug previously used to treat Ebola. It is a pro-drug nucleoside with antiviral activity that is opposed to SARS-CoV-2 and coronavirus. Aim: Current research was planned to evaluate and compare the potential ameliorative impact of the hematopoietic-stem-cell mobilized by the granulocyte colony-stimulating factor (G-CSF) versus BM-MSC on the effect of novel antiviral remdesivir on the kidney. Materials and Methods: Rats divided into four groups: control group, Remdesivir treated group (20 mg/kg/day IV on the first day followed by 10 mg/kg/day for 6 days), Remdesivir + BM-MSCs group (3x10⁶ cells/ml of PKH26 labelled MSC) and Remedesivir+ Filgrastim group (70 μg/kg/day/5 days). At the end of the experiment, animals were anaesthetized and sacrificed. Both animal kidneys were excised for histological, immunohistochemistry, and electron microscopy studies. Biochemical and morphometric assessments had been performed. Results: Remdesivir caused distortion and degeneration of both the glomeruli and the renal tubules associated with Bowman's space widening. It greatly increased the deposition of collagen and enhanced the expression of caspase 3, IL-6, and TGF-β1. Ultrastructure changes were observed in the form of thickening of glomerular basement membrane, dilated basal plasma membrane infoldings of tubular epithelium and mitochondrial degeneration. Biochemically, decreased antioxidant enzymes, reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) with increased serum urea and creatinine were also recorded. Both BM-MSCs and G-CSF improved histological structure and function of the kidney. Conclusion:Prescribing drugs such as remdesivir should be carried out with severe care. BM-MSCs and G-CSF are an efficient and ideal option to protect patients from irreversible kidney damage.

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Section: Mobilizationsupporting

confidence: 84%

Impact of Remdesivir on the kidney and potential protective capacity of Granulocyte-Colony Stimulating Factor versus Bone Marrow Mesenchymal Stem Cells in adult male albino rats

El-Haroun

Bashandy

Soliman

2021

Egyptian Journal of Histology

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“…Regarding vascular alterations, consistent with our results, other studies have reported that different nanoparticles with different sizes resulted in expanded and congested renal tubular capillaries with inflammatory infiltration [ 29 , 32 ]. It has been reported that cell infiltration is a sign of atrophy of tubular cells in chronic kidney diseases [ 38 ]. This inflammatory response seems to be a result of the oxidative stress caused by AgNPs, contributing to vascular congestion.…”

Section: Discussionmentioning

confidence: 99%

The potential renal toxicity of silver nanoparticles after repeated oral exposure and its underlying mechanisms

et al. 2021

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Background Silver nanoparticles (AgNPs) can accumulate in various organs after oral exposure. The main objective of the current study is to evaluate the renal toxicity induced by AgNPs after repeated oral exposure and to determine the relevant molecular mechanisms. Methods In this study, 40 male Wistar rats were treated with solutions containing 30, 125, 300, and 700 mg/kg of AgNPs. After 28 days of exposure, histopathological changes were assessed using hematoxylin-eosin (H&E), Masson’s trichrome, and periodic acid-Schiff (PAS) staining. Apoptosis was quantified by TUNEL and immunohistochemistry of caspase-3, and the level of expression of the mRNAs of growth factors was determined using RT-PCR. Results Histopathologic examination revealed degenerative changes in the glomeruli, loss of tubular architecture, loss of brush border, and interrupted tubular basal laminae. These changes were more noticeable in groups treated with 30 and 125 mg/kg. The collagen intensity increased in the group treated with 30 mg/kg in both the cortex and the medulla. Apoptosis was much more evident in middle-dose groups (i.e., 125 and 300 mg/kg). The results of RT-PCR indicated that Bcl-2 and Bax mRNAs upregulated in the treated groups (p < 0.05). Moreover, the data related to EGF, TNF-α, and TGF-β1 revealed that AgNPs induced significant changes in gene expression in the groups treated with 30 and 700 mg/kg compared to the control group. Conclusion Our observations showed that AgNPs played a critical role in in vivo renal toxicity.

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“…Previous researchers contributed this finding and the observable interrupted basal laminae to ROM generation which led to rapid loss of cytoskeletal integrity. [37]…”

Section: Discussionmentioning

confidence: 99%

Effect of suramin on renal proximal tubular cells damage induced by cisplatin in rats (histological and immunohistochemical study)

Elkordy

2019

J Microsc Ultrastruct

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Background:Renal toxicity is the most common complication of cispaltin therapy that has broad-spectrum antitumor activity against a variety of human solid tumor. Suramin, a Food and Drug Administration-approved old drug is a polysulfonated compound of napthylurea originally designed to treat trypanosomiasis.Aim:The current work aimed to investigate the possible protective effect of different doses of suramin against cisplatin-induced renal proximal tubular cells (RPTCs) damage.Material and Methods:Fifty adult male rats were used and divided into five equal groups. Group I served as a control, group II received suramin alone (10 mg/kg). Groups III, IV and V were administered cisplatin once (5 mg/kg, intraperitoneally) alone or combined with low dosage suramin (5 mg/kg) or high dosage suramin (10 mg/kg) once intravenously respectively.Results:Compared with control rats, cisplatin administration caused proximal tubules damage, RPTCs vacuolation with pyknotic nuclei, loss of brush border and widespread caspase-3 immunostaining. Cisplatin-induced RPTCs toxicity was further confirmed morphometrically (a significantly decreased proximal tubular epithelium height and increased mean number of caspase-3-immunopositive cells). These changes were accompanied by biochemical alteration manifested as a significant increase of blood urea nitrogen and serum creatinine. Simultaneous administration of high-dose but not low-dose suramin to the cisplatin-treated rats improved the deleterious morphological and morphometrical effects on RPTCs and restored the aforementioned biochemical parameters to control values.Conclusion:In conclusion suramin in a dose dependant manner protects RPTCs from damage induced by cisplatin.

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Histological study on the protective effect of endogenous stem-cell mobilization in Adriamycin-induced chronic nephropathy in rats

Cited by 12 publications

References 35 publications

Impact of Remdesivir on the kidney and potential protective capacity of Granulocyte-Colony Stimulating Factor versus Bone Marrow Mesenchymal Stem Cells in adult male albino rats

Impact of Remdesivir on the kidney and potential protective capacity of Granulocyte-Colony Stimulating Factor versus Bone Marrow Mesenchymal Stem Cells in adult male albino rats

The potential renal toxicity of silver nanoparticles after repeated oral exposure and its underlying mechanisms

Effect of suramin on renal proximal tubular cells damage induced by cisplatin in rats (histological and immunohistochemical study)

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