RESUMO
Chronic kidney disease is a global health problem with increasing morbidity and mortality. Therefore, this study was planned to test the protective effect of hematopoietic-stem-cell mobilization by granulocyte colony-stimulating factor (G-CSF) on Adriamycin (ADR)-induced chronic renal disease in rats. Thirty albino rats were equally divided into three groups: control, ADR group [rats received a single intravenous injection of ADR (5 mg/kg)], and G-CSF group [rats received ADR by the same route and the same dose as the previous group, and then G-CSF (70 µg/kg/d) 2 hours after ADR injection then daily for five consecutive days]. At the time of sacrifice (after 6 weeks), blood samples were taken to estimate the blood urea nitrogen and serum creatinine. Kidney sections were stained with hematoxylin and eosin, toluidine blue, Masson's trichrome, periodic acid-Schiff stains, and immunohistochemical staining against CD34 and caspase-3. The G-CSF group exhibited protection against renal injury manifested by reducing blood urea nitrogen and serum-creatinine levels, improving histological architecture, and increasing the proliferative capacity of renal tubules.
RESUMO
BACKGROUND AND OBJECTIVES: Acute kidney injury (AKI) represents a major clinical problem with high mortality and limited treatment protocols. This study was planned to evaluate the therapeutic effectiveness of bone marrow - derived mesenchymal stem cells (BM-MSCs) in a rat model of ischemia/reperfusion (I/R) AKI. METHODS AND RESULTS: This study was carried out on thirty adult male albino rats. Animals were divided equally into three groups. Group I (control sham-operated group) (n=10), were subdivided equally into two subgroups; Ia and Ib. The experimental group (n=20) were all subjected to I/R injury by clamping both renal pedicles for 40 minutes. Half of the I/R animals did not receive MSC therapy (group II) [non-MSC treated group]. The other half of the I/R animals received single intravenous injection of PKH26 labelled BM-MSCs immediately after removal of the clamps and visual confirmation of reflow (group III) [MSC treated group]. Animals were sacrificed 24 hrs (subgroups IIa & IIIa) and 72 hrs (subgroups IIb & IIIb) after intervention. Serological measurements included serum urea and creatinine. Kidney specimens were processed for H&E, PAS and PCNA. Mean % of renal corpuscles with affected glomeruli, mean % of affected tubules, mean area % of PAS-positive reaction and mean area % of PCNA immunoreactivity were measured by histomorphometric studies and statistically compared. MSCs-treated group exhibited protection against renal injury serologically and histologically. CONCLUSIONS: Results of the present study suggest a potential reno-protective capacity of MSCs which could be of considerable therapeutic promise for cell-based management of clinical AKI.
