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Introduction: Acute kidney injury (AKI) is a syndrome of rapidly declining renal function. Cisplatin nephrotoxicity is a major cause of AKI in about one third of patients under cisplatin treatment. Stem cell therapy have been suggested as a protective measure against cisplatin-induced AKI. The conditioned medium of the stem cells (serum-free culture medium) has been also found to minimize renal injury and might develop a new therapeutic strategy that avoids stem cells administration. Aim of the Study:This study was conducted to compare the effect of intravenous injection of bone marrow-derived mesenchymal stem cells (BMSCs) versus their conditioned medium (CM) in minimizing the cisplatin-induced acute renal injury. Material and Methods: Sixty adult female albino rats were divided into 4 main groups. Group (I) served as a control group, Group (II) (cisplatin treated group) that were subdivided into two subgroups IIa and IIb, Group (III) (BMSCstreated group) and Group (IV) (CM-treated group). Five young male rats were additionally used for obtaining the BMSCs. Rats of all groups were sacrificed on 4th day of the experiment, except for the rats of subgroup (IIa (which were sacrificed after one day of cisplatin administration. Renal specimens were prepared for histological and immunohistochemical techniques. Morphometrical studies and statistical analysis were performed. Results: Treatment by BMSCs resulted in obvious improvement of renal structure with significant increase in Proliferating Cell Nuclear Antigen (PCNA). However, conditioned medium (CM) was less effective in treatment of acute AKI. Conclusion: BMSCs administration is preferable than their CM in reversing the acute structural damage of the kidney induced by cisplatin.

Hyperuricemia was linked to diabetes mellitus, metabolic syndrome, and oxidative stress, and could be induced by higher fructose consumption through altering energy status in liver. l‐Carnitine is an antioxidant, affecting mitochondria and cellular energetics; however, little is known about its effects in hyperuricemic states. This study investigated metabolic and hepatic effects of hyperuricemia and fructose feeding, and demonstrated the role of l‐Carnitine in such states. Fifty adult male Wistar rats were randomly divided into control, untreated hyperuricemic, fructose‐supplemented hyperuricemic, l‐Carnitine‐treated hyperuricemic, and l‐Carnitine‐treated fructose‐supplemented hyperuricemic groups. The separated plasma was used for determination of the glycemic control, lipid profile, liver function tests, uric acid level, and oxidative stress markers. Atherogenic index, HOMA‐IR, and body mass index (BMI) were calculated. Left liver lobe and left kidney specimen from all groups were used for histopathological studies. Hyperuricemic rats exhibited significantly hypoalbuminemia, dyslipidemia, insulin resistance, and oxidative stress compared to the controls. Fructose‐supplemented hyperuricemic group showed obesity and more deleterious effects, as well as, steatosis, and renal tubular damage compared to the hyperuricemic rats. Concomitant l‐Carnitine treatment with hyperuricemia improved such effects, despite causing adiposity. While combined l‐Carnitine treatment and fructose supplementation in hyperuricemia limited the aggressive hyperuricemic picture of fructose supplementation. It is concluded that hyperuricemia has detrimental metabolic and hepatic effects. Artificial fructose supplementation worsened such effects, while l‐Carnitine was efficient in ameliorating these hyperuricemia and/or excess fructose‐induced hyperuricemia effects, through its anti‐inflammatory, antisteatotic, and antioxidant properties.

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Background Repairing urinary bladder (UB) defect by enterocystoplasty remains the gold standard surgical bladder reconstruction procedure to increase the capacity and compliance of dysfunctional bladders. However, many complications were recorded. Aim of the work This work aimed to compare the consequences of reconstruction of urinary bladder defect using untreated small intestinal submucosal (SIS) matrix versus seeded and unseeded decellularized SIS matrix. Material and Methods Fifty female albino rats were used in this study. The animals were divided into three groups: Group I (Control) included ten adult rats from which ileal tissue was obtained. Group II included ten adult rats in which their UB defect was repaired by untreated cellular SIS. Group III included twenty adult rats that were subdivided into two subgroups, 10 rats each; Subgroup IIIA where rats had their UB defect repaired by acellular SIS and subgroup IIIb where rats had their UB defect repaired by acellular SIS seeded with adipose mesenchymal stem cells (AMSCs).Ten young rats were used for preparation of AMSCs. Morphometric and statistical analysis were also performed. Results In rats where UB defect was repaired by untreated cellular SIS, the graft area showed loss of epithelial polarity, presence of intraepithelial cysts and occasional extension of urothelium to the outer surface forming fistula. There were areas of metaplasia with the appearance PAS positive cells. In the lamina propria, there was areas of lymphocytic infiltration together with significant increase in the collagen fiber deposition (p < 0.05). There was a significant decrease thickness of muscle layer as compared to control (p < 0.05). In rats where UB defect was repaired by acellular SIS, urothelium in the graft area showed occasional squamous metaplasia and often the urothelium extended to the deeper layers forming Brunn's nest. There was minimal muscle regeneration in the graft area. However, in rats where UB defect was repaired by acellular SIS seeded with AMSCs, the urothelium in the graft area was nearly similar to control group with uniform urothelium thickness, minimal collagen fibers deposition and thick muscle layer that showed no significant difference from the control (p > 0.05). Conclusion Acellular SIS seeded with AMSCs showed better results compared to non-seeded and cellular SIS in reconstructing urinary bladder defects.