Background and objectives: Adipose tissue is an abundant and easily accessible tissue for obtaining multipotent stem cells that harbor similar phenotypes to bone marrow mesenchymal stem cells. This study aimed to demonstrate the effect of adiposederived mesenchymal stem cells (AD-MSCs) on repairing the aspirin-induced gastric ulcer (GU). Materials and Methods: The gastric ulcer in rats was induced by oral dose of 100 mg/kg aspirin for 3 days. AD-MSCs isolated from male rats were transplanted into female rats via tail vein injection. Healing of the GU was monitored histologically. Homing of the in vivo administration of MSCs was assessed by PCR detection of SRY gene and immunohistochemical detection of CD44 in gastric mucosa. Results: At 72 hours after AD-MSCs transplantation, there was complete restoration of the fundic glands with marked reduction in inflammatory cellular infiltrate and a significant increase in the mean value of optical density of PAS positive area (P < 0.05). The mean number of CD44 positive cells in the gastric mucosa was significantly increased (P < 0.05). SRY-specific gene of Y chromosome was detected in female rat gastric mucosa. Conclusions: In vivo transplantation of AD-MSCs accelerate healing of GU in a rat model of gastric injury.

Background: Traditional therapeutic strategies used for the treatment of acute kidney injury (AKI) proved to be less effective in reducing the morbidity and mortality rate. Recently, stem cell therapy showed a promise for treatment of this complex disorder. Aim: To investigate the therapeutic role of adipose-derived mesenchymal stem cells (AD-MSCs) in treatment of cisplatininduced nephrotoxicity as a model of AKI. Material and Methods: Twenty adult female Wister rats were divided equally into four groups. Group I was the control, the other three groups received a single intraperitoneal injection of cisplatin (5 mg /kg), where group II were sacrificed after one day from cisplatin injection, group III were sacrificed after seven days from cisplatin injection and group IV received adult male rat AD-MSCs (2x106 cells/rat) in tail vein one day after cisplatin injection and were sacrificed seven days after cisplatin injection. Results: The histopathological changes in the renal cortex were more obviously detected in group III than in group II. These changes include congested and shrunken glomeruli, dilated Bowman's space and loss of proximal convoluted tubules brush borders. Moreover, distal tubular cells showed cytoplasmic vacuolization, with pyknotic nuclei and presence of intraluminal hyaline casts. Interstitial collagen deposition was also noticed. In group IV, AD-MSCs administration almost restores the renal histological architecture. Increased tubular cell proliferation with marked reduction of the interstitial inflammation and fibrosis were also detected. However, some renal glomeruli and tubules showed degenerative changes. Male rat derived-stem cells were detected in the female kidney tissue by Y chromosome PCR technique. Conclusion: Administration of AD-MSCs had a potential regenerative effect for the management of AKI.

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Purpose: This study was designed to evaluate the possible nephroprotective and therapeutic role of bone marrow mesenchymal stem cells (BMSCs) in comparison to vitamin C in a rat model of gentamicin (GM) induced nephrotoxicity. Materials and Methods: Forty adult male Wistar rats (150-200 gm) were used in this study. Five rats were utilized to obtain BMSCs and thirty-five rats were divided into: Group I: control, Group II (GM): received 100mg/kg GM intramuscularly for 8 days, subdivided into: subgroup IIa (GM toxicity): sacrificed after the last dose of GM; and subgroup IIb (GM recovery): sacrificed 8 days after the last injection; Group III (Protection): subdivided into: subgroup IIIa (BMSCs protection): received a single intravenous (IV) injection of BMSCs with the first dose of GM and subgroup IIIb (Vitamin C protection): received 200mg/kg vitamin C intraperitoneal (IP) for 8 days simultaneously with the daily GM doses; and Group IV (Treatment): subdivided into: subgroup IVa (BMSCs treatment): received single IV injection of BMSCs after the last dose of GM and subgroup IVb (Vitamin C treatment): received 200mg/kg vitamin C IP for 8 days after the last dose of GM. Serum creatinine and urea were measured, and kidneys were processed for histological, immunohistochemical and morphometric studies. Results: GM resulted in vacuolation, desquamation of tubular epithelium, interstitial inflammation, congestion and increased number of PCNA positive cells. Serum creatinine and urea were significantly increased. Vitamin C administration, either as a treatment or protection, significantly ameliorated these changes. Conversely, BMSCs could not prevent the GM toxicity but exerted a therapeutic role. Conclusion: BMSCs had no role in protection against GM nephrotoxicity, whereas, their administration after kidney injury assisted kidney regeneration. However, vitamin C exhibited a dual significant role in prevention and improvement in kidney structure and biochemical results.

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