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1.
International Journal of Stem Cells ; : 115-124, 2012.
Artigo em Inglês | WPRIM | ID: wpr-69146

RESUMO

BACKGROUND AND OBJECTIVES: Glomerulosclerosis develops secondary to various kidney diseases. It was postulated that adriamycin (ADR) induce chronic glomerulopathy. Treatment combinations for one year did not significantly modify renal function in resistant focal segmental glomerulosclerosis (FSGS). Recurrence of FSGS after renal transplantation impacts long-term graft survival and limits access to transplantation. The present study aimed at investigating the relation between the possible therapeutic effect of human mesenchymal stem cells (HMSCs), isolated from cord blood on glomerular damage and their distribution by using ADR induced nephrotoxicity as a model in albino rat. METHODS AND RESULTS: Thirty three male albino rats were divided into control group, ADR group where rats were given single intraperitoneal (IP) injection of 5 mg/kg adriamycin. The rats were sacrificed 10, 20 and 30 days following confirmation of glomerular injury. In stem cell therapy group, rats were injected with HMSCs following confirmation of renal injury and sacrificed 10, 20 and 30 days after HMSCs therapy. Kidney sections were exposed to histological, histochemical, immunohistochemical, morphometric and serological studies. In response to SC therapy multiple Malpighian corpuscles (MC) appeared with patent Bowman's space (Bs) 10 and 20 days following therapy. One month following therapy no remarkable shrunken glomeruli were evident. Glomerular area and serum creatinine were significantly different in ADR group in comparison to control and SC therapy groups. CONCLUSIONS: ADR induced glomerulosclerosis regressed in response to cord blood HMSC therapy. A reciprocal relation was recorded between the extent of renal regeneration and the distribution of undifferentiated mesenchymal stem cells.


Assuntos
Animais , Humanos , Masculino , Ratos , Creatinina , Doxorrubicina , Sangue Fetal , Glomerulosclerose Segmentar e Focal , Sobrevivência de Enxerto , Rim , Nefropatias , Transplante de Rim , Células-Tronco Mesenquimais , Recidiva , Regeneração , Células-Tronco , Transplantes
2.
International Journal of Stem Cells ; : 130-139, 2012.
Artigo em Inglês | WPRIM | ID: wpr-69144

RESUMO

BACKGROUND AND OBJECTIVES: It was postulated that adriamycin (ADR) induce renal tubulointerstitial injury. Clinicians are faced with a challenge in producing response in renal patients and slowing or halting the evolution towards kidney failure. The present study aimed at investigating the relation between the possible therapeutic effect of human mesenchymal stem cells (HMSCs), isolated from cord blood on tubular renal damage and their distribution by using ADR induced nephrotoxicity as a model in albino rat. METHODS AND RESULTS: Thirty three male albino rats were divided into control group, ADR group where rats were given single intraperitoneal (IP) injection of 5 mg/kg adriamycin. The rats were sacrificed 10, 20 and 30 days following confirmation of tubular injury. In stem cell therapy group, rats were injected with HMSCs following confirmation of renal injury and sacrificed 10, 20 and 30 days after HMSCs therapy. Kidney sections were exposed to histological, histochemical, immunohistochemical, morphometric and serological studies. In response to SC therapy, vacuolated cytoplasm, dark nuclei, detached epithelial lining and desquamated nuclei were noticed in few collecting tubules (CT). 10, 20 and 30 days following therapy. The mean count of CT showing desquamated nuclei and mean value of serum creatinine revealed significant difference in ADR group. The mean area% of Prussian blue+ve cells and that of CD105 +ve cells measured in subgroup S1 denoted a significant increase compared to subgroups S2 and S3. CONCLUSIONS: ADR induced tubulointerstitial damage that regressed in response to cord blood HMSC therapy.


Assuntos
Animais , Humanos , Masculino , Ratos , Creatinina , Citoplasma , Doxorrubicina , Sangue Fetal , Rim , Células-Tronco Mesenquimais , Insuficiência Renal , Células-Tronco
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