Background: Central nervous system (CNS), in particular, depends on thyroid hormones (TH) for the growth and upkeep of normal physiological processes. The preferred medication for thyroid replacement therapy continues to be levothyroxine, a synthetic thyroid hormone.
Objectives: The goal of the current study was to determine whether maternally induced hypothyroidism could have an impact on the postnatal development of albino rat visual cortex and whether levothyroxine might have any protective effects or not.
Material and Methods: Twenty one (21) pregnant rats were randomly divided equally into three groups; control group (received distilled water orally daily from first day of gestation until day 20 after delivery), hypothyroid group (received Carbimazole orally in a dose of 5 mg/rat/ day from first day of gestation until day 20 after delivery) and hypothyroid group treated with levothyroixine (received Carbimazole orally in a dose of 5mg/ rat/ day for the same period concomitantly with Levothyroxine subcutaneously at a dose of 5µg/day/rat from day 10 of gestation until 20 day after delivery). Pups (newborn, 10 and 20 days) were anesthetized, sacrificed; their brains were processed for histological evaluation. Morphometric and statistical studies were done.
Results: Hypothyroidism induced visual cortex histological insults in the form of decreased cortical thickness and nuclear size and increase in packing of cells. Darkly stained cells were noticed. Clustering of pyramidal cells in ganglionic layer was not evident. Borders between layers couldn’t be easily distinguished. These insults were ameliorated in hypothyroid rats treated with Levothyroxine.
Conclusion: Levothyroxine might protect against maternal hypothyroidism induced visual cortical neurotoxicity.
Background Multiple sclerosis (MS) is the commonest demyelinating degenerative disease causing adult neurological disability. The cuprizone (CPZ) model is suitable for studying MS induced demyelination. Thymoquinone (TQ) and Platelet rich plasma derived lyophilized growth factors (PRP d. LGFs) showed neuroprotective activity and had been successfully applied in degenerative conditions.
Aim of the work to determine and compare the possible neuroprotective activities for TQ and LGFs against CPZ induced demyelination in rat corpus callosum (CC).
Material and methods 40 male adult albino rats were randomly and equally assorted in 4 groups; Group I (Control group): The rats received nothing. Group II (CPZ group): The rats fed standard rodent chow mixed with 0.6% CPZ/ day (0.6 g of Cuprizone was added to 100 g of chow) for 4 weeks. Group III (CPZ + TQ): The rats were given 0.6% CPZ and TQ daily (20 mg/ kg body weight) dissolved in corn oil (0.5 ml/ rat) orally by intragastric tube for 4 weeks. Group IV (CPZ + PRP d. LGF): The rats received 0.6% CPZ and LGF (250 μL dissolved in distilled water, by intraperitoneal injection) 2 times every week in 4 weeks. At the distend time, light microscopic, electron microscopic, immunohistochemical and morphometric studies were used to study myelination and demyelination in rat CC.
Results: Cuprizone induced oligodendrocytes damage or loss in the rat CC with a subsequent loss of myelin, axonal degeneration and astrogliosis. Both LGFs and TQ attenuated the CPZ induced CC demyelination, but it was more obvious in the LGFs treated group.
Conclusion: Simultaneous administration of LGF or TQ with CPZ improved CC architecture in CPZ model of demyelination with higher protective efficacy for LGF over TQ.
Discussion of the master's thesis of Dr. Youssef Youssef, resident physician in the Department of Internal Medicine, Faculty of Medicine, Assiut University
Background: Bone marrow-derived mesenchymal stem cells (BM-MSCs) offer promising regenerative therapy potential. This study compared the effects of BM-MSCs and α-tocopherol (α-Toc) on apoptosis, autophagy, β-cell function, and associated signaling pathways in a streptozotocin (STZ)-induced diabetes rat model. Additionally, it explored the entero-insular axis and PI3K/Akt signaling.
Methods: Forty adult male albino rats were divided into four groups: control, diabetic (STZ-induced, 45 mg/kg), diabetic treated with BM-MSCs, and diabetic treated with α-Toc. Blood glucose, insulin, nitric oxide (NO), and catalase (CAT) levels were measured. Pancreatic histopathology, expression of insulin, CD44, caspase-3, autophagy markers, PI3K/Akt signaling, pancreas/duodenum homeobox protein 1, and glucose-dependent insulinotropic polypeptide (GIP) were analyzed using histological and molecular techniques.
Results: Diabetic rats showed elevated glucose levels, impaired GIP expression, and partial restoration of pancreatic islets. Both BM-MSCs and α-Toc treatment improved autophagy, restored PI3K/Akt signaling, and reversed intestinal GIP expression. However, BM-MSCs demonstrated superior cytoprotective effects compared to α-Toc.
Conculsion: These findings suggest that BM-MSCs and α-Toc have therapeutic potential in type 1 diabetes by targeting autophagy, β-cell function, and entero-insular axis regulation, with BM-MSCs offering a more pronounced effect.
Vitiligo is a chronic depigmenting disorder with multiple aetiopathogenic theories. Weak expression of epithelial cadherin protein has been implicated as an aggravating factor in the selective loss of melanocytes in affected skin areas. Yet, little information is known about the role of the cadherin gene as a susceptible gene to vitiligo.
We assessed the association between genetic polymorphism of the Cadherin (CDH1)-encoding gene and the risk of developing vitiligo in Egyptians.
Venous blood samples were obtained from 25 vitiligo patients and 25 healthy controls. Total DNA extraction was performed followed by a single nucleotide polymorphism genotyping assay of CDH1C/T (rs10431924) gene using real-time PCR. Vitiligo patients were clinically evaluated.
An insignificant association between the CDH1 (rs10431924) genotypes or allele distribution, and the risk of developing vitiligo was observed after comparing patients and controls.
In contrast to the previous studies, we did not detect the CDH1 (rs10431924) gene polymorphism as a risk factor for acquiring vitiligo.
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