Multiple sclerosis (MS) is an autoimmune inflammatory neurodegenerative disease of the central nervous system (CNS) that disrupts the myelin sheath, leading to dysfunction of the brain and spinal cord. No curative treatment is known for MS. Mesenchymal stem cells, through their immunomodulatory effects, represent a promising therapeutic approach for MS. The aim of this article is to explore the impact of human adiposederived mesenchymal stem cells (ASCs) on chronic experimental autoimmune encephalomyelitis (EAE) model of MS when injected after a disease entered an irreversible clinical course. Forty-one female albino rats were classified into the following groups: I: control, II: EAE-untreated, III and IV: EAE treated with PBS at 15 and 25 days postimmunization (dpi), respectively, V and VI: EAE treated with ASCs at 15 and 25 dpi, respectively. Intravenous administration of ASCs at 15 or 25 dpi significantly ameliorates the disease course and decreases the immune cell infiltration, vascular congestion and axonal loss of the gray and white matters of cerebral cortex. ASCs treatment induced a Th2 shift of the immune response and downregulation of IL-17 levels. We also found an engraftment of the ASCs into the lymph nodes and the brains up to 25 days after injection. The important finding was that human HLA-G gene was significantly expressed in lymph nodes and brains of rats treated with ASCs. Transplantation of human ASCs has demonstrated striking therapeutic effects and unique immunomodulatory capacities when delivered at the peak or later in the course of the disease in EAE rats. Interestingly, ASCs injection at the peak of EAE had better effects Conflict of interest: Nothing to report.
Background: Being a highly immature organ at birth, the rat kidney is morphologically as fetal when compared with humans. Events that occur during fetal development might determine adult renal diseases. Aim of work: This study aimed to characterize the postnatal developmental changes of the kidneys in albino rats using light microscope from postnatal day (PND) 2 until PND 70. This may give references to pathologists when evaluating juvenile toxicology studies. Materials and Methods: Ten healthy pregnant albino rats were used in this study. Twenty-five of their offsprings were obtained and divided according to age into five groups of 5 pups each. Group A: studied at PND 2. Group B: studied at PND 10. Group C: studied at PND 20. Group D: studied at PND 30. Group E: studied at PND 70. Kidneys were removed, processed for light microscopic study and 5 m thick paraffin sections were obtained and stained with hematoxylin and eosin stain. Results: Light microscopic examination of the renal cortex at PND 2 revealed subcapsular nephrogenic zone contained immature renal developmental stages, juxtamedullary zone contained formed glomeruli with medullary rays between the two zones. The renal cortex acquired maturation centrifugally with the superficial nephrons was the last to mature by PND 20. The papilla was the most mature region of the kidney and at PND2; it had the structural composition of the inner stripe of outer medulla. The papillary maturation involved a process of tubular elongation and increase in the interstitium until reaching adult structure by PND 20. At PND 2, the medulla was the most immature zone being formed of islets of tubular structures among abundant interstitium with high degree of undifferentiation. Its maturation involved tubular elongation and decrease of the interstitium with the outer medulla was the last to mature as late as PND 30. Consequently, the medulla remained immature for a relatively long postnatal period, in comparison to the other kidney regions. Conclusion: It was concluded that, rat kidney is immature at birth and kidney sub regions mature at different rates during postnatal development. The papilla was the first to mature (PND 20) followed by the cortex (PND 20) and finally the medulla (PND 30).
Tacrolimus is a powerful immunosuppressive agent with hepatotoxic and nephrotoxic effects. It has a protective role against many toxicants. This study was conducted to evaluate the possible protective role of spirulina against tacrolimus induced hepatotoxicity and nephrotoxicity. Forty adult male albino rats divided into 4 groups. Group I, control group, Group II, spirulina group (received spirulina 500 mg/Kg body weight (bw)/day orally), Group III, tacrolimus group (received tacrolimus 12 mg/kg bw/day orally); and Group VI, prophylactic group (orally administered spirulina for 3 days before and 28 days concurrently with tacrolimus in the same previous doses). Tacrolimus induced adverse effects on both liver and kidney functions and structure that was manifested by elevated hepatic transaminases, total and direct bilirubin, albumin, blood urea nitrogen, serum creatinine and creatinine clearance. There was a significant decrease in serum total antioxidant capacity (TAC) and hepatic and renal total thiol molecules (TTM), with a significant increase in serum malondialdehyde in tacrolimus group. Histopathologically, tacrolimus induced swelling and granulation of hepatocytes, congestion of blood sinusoids and degeneration of bile ductiles, glomerular hypertrophy and segmentation, swelling, degeneration and hyalinosis of renal tubules. Spirulina pre-and co-treatment significantly improved these deleterious effects. This was accompanied by partial restoration of the expression of PCNA near to the normal level observed in control rats. Moreover, spirulina treatment did not alter the trough blood tacrolimus levels or tacrolimus-induced immunosuppression. Further studies are warranted to evaluate whether transplant patients on tacrolimus treatment may benefit from the protective effects of spirulina.
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