We designed this work to examine the curative role of L-carnitine (LCAR) in a rat model of cisplatin (CDDP)-induced kidney injury. We induced kidney injury in rats by a single intraperitoneal injection of 5 mg/kg of CDDP. Fifteen days post injection, rats were orally supplemented with 354 mg/kg of LCAR for another 15 days. Kidney tissues were subjected to histo-biochemical analysis along with mRNA gene expression quantification for cytoskeleton proteins encoding genes (vimentin, nestin, and connexin 43) by real-time reverse transcription polymerase chain reaction. LCAR reversed CDDP-induced renal structural and functional impairments. LCAR significantly declined serum urea and creatinine concentrations, restored oxidant/antioxidant balance, reversed inflammation, and antagonized caspase 3-mediated apoptotic cell death in renal tissues. Moreover, LCAR effectively down-regulated cytoskeleton proteins mRNA levels, reflecting amelioration of CDDP-provoked podocyte injury. We concluded that LCAR has a favorable therapeutic utility against CDDP-induced kidney injury.

Background: Male infertility is considered a major cause of couple infertility as it represents 25- 50 % of infertility cases. In addition, non-obstructive azoospermia (NOA) represents 10% of all infertile men.There is no definite curable treatment for such cases. Aim of Work: The purpose of this research was to assess the efficacy of BM-MSCs and AT-MSCs in treating busulfan-induced azoospermia in wistar rats. Materials and Methods: BM-MSCs were extracted from the femur bones of five adult Wistar rats and AT-MSCs from preperitoneal adipose tissue. They were then evaluated for morphology, MSC markers, osteogenic and adipogenic differentiation. To produce azoospermia in male Wistar rats, two doses of busulfan (15 mg/kg and 30 mg/kg) were administered intraperitoneally during a 21-day period. The seminiferous tubules of each testis were injected with 2.5106 MSCs 35 days after the second busulfan injection. 12 weeks after cell therapy, the testes were examined histopathologically and histomorphometrically. Results: Like the control group, the seminiferous tubules treated with BM-MSCs demonstrated normal spermatogenesis in compared to the busulfan-induced azoospermic testes. In contrast to the busulfan-induced azoospermic testes, the seminiferous tubules treated with AT-MSCs exhibited a practically typical look of spermatogenesis. Conclusion: BM-MSCs and AT-MSCs were shown to be beneficial in treating azoospermia in the wistar rat model, restoring fertility to busulfan-induced azoospermic animals after MSC transplantation. As a result, this discovery may pave the way for the future use of MSCs in the treatment of human azoospermia, although more research should be conducted to confirm the findings.