Background and ObjectivesAlzheimer’s disease (AD) is a devastating neurodegenerative disorder. Increasing evidence implicates diabetes mellitus (DM) as a risk factor for AD. Green tea (GT) has several beneficial effects attributed to its anti-oxidant phenolic compounds. Adipose tissue is a rich source of adipose-derived mesenchymal stem cells (ADSCs). This study was designed to evaluate and compare the possible therapeutic effect of green tea extract (GTE) and ADSCs on AD complicating induced DM in male rat.Methods31 adult male albino rats were divided into 5 groups. Group I (Control), Group II received GTE, 50 mg/kg daily orally for 4 weeks, Group III received a single intraperitoneal injection of Streptozotocin (STZ), 50 mg/kg, Group IV: received STZ followed by GTE and Group V: received STZ followed by human ADSCs (hADSCs) intravenously.ResultsMultiple acidophilic masses, deformed neurons, Congo red +ve masses and Caspase 3 +ve neurons were seen in group III, became few in group IV and occasional in group V. Multiple Prussian blue +ve cells were detected in group V. Some CD44 +ve cells were noticed in group III, became multiple in groups IV and V. The mean area of neurons exhibiting acidophilic cytoplasm, mean area of amyloid plaques and mean area % of Caspase 3 +ve cells indicated a significant increase in group III. The mean area % of CD44 +ve cells recorded a significant increase in group IV.ConclusionshADSCs exerted a more marked therapeutic effect on the neurodegenerative changes complicating DM and corresponding to AD.

Background Adult-onset hypothyroidism has a deleterious effect on hippocampal cognitive and memory functions. This study was performed to evaluate the possible therapeutic effect of thyroxine on hippocampus degeneration in an adult male rat model of carbimazole-induced hypothyroidism and the potentiality of spontaneous recovery. Thirty-two adult male albino rats were divided equally into four groups, as follows: I (control group), II (hypothyroidism group) received carbimazole (20 mg/kg) orally once daily for 4 weeks; III (recovery group) rats were managed as in group II, then left untreated for an additional 4 weeks to assess spontaneous recovery; and IV (thyroxine-treated group): hypothyroidism was induced as in group II, then rats received levothyroxine (20 µg/kg/day) orally for 4 weeks. Rats and their corresponding controls were sacrificed after 4 weeks in group II and after 8 weeks in groups III and IV. The levels of T3, T4, and TSH were measured. Hematoxylin and Eosin staining of thyroid and hippocampal sections was performed. Additionally, toluidine blue staining and immunohistochemical staining for PCNA, GFAP, and synaptophysin were applied to hippocampus sections. Both morphometric measurements and statistical analysis were performed. Results Comparison of thyroxine-treated group with hypothyroidism and recovery groups revealed a significant reduction in TSH  level and an increase in T3 and T4 levels, as well as improved histological architecture in both the thyroid and hippocampal sections. Hippocampal sections revealed a significant decrease in the mean area percent of GFAP, a significant increase in the mean number of PCNA-positive cells in the subgranular zone (SGZ); a niche for the adult neural stem cells (NSCs) in the hippocampus; and a significant increase in the mean area percent as well as the mean optical density of synaptophysin. Conclusion Hippocampal degeneration is induced by hypothyroidism and can be restored by thyroxine replacement therapy, probably through neuronal cell preservation, synaptogenesis, and stimulation of neurogenesis in SGZ. On the other hand, spontaneous recovery from this degeneration was inadequate.

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Introduction: Psoriasis is an autoimmune skin disorder that is symptomized by erythema and scaling. Recently, imiquimod (IMQ) has been used to induce skin inflammation in mice to create a psoriasis model. Aim of the Work: To assess the possible preventive potential of acarbose on psoriasis-like skin inflammation induced by IMQ in adult male mice, and to compare it to calcipotriol/betamethasone applied on the same psoriasis mouse model. Materials and Methods: Thirty four BALB/c mice were classified as the following groups: I(Control), II(IMQ): IMQ-model with topically applied Aldara cream, ІII(Acarbose): IMQ-model treated with Glucobay orally, ІV(Calcipotriol/Betamethasone): IMQ-model treated with Calcipoheal-Cort ointment and V(Acarbose+Calcipotriol/Betamethasone): IMQ-model treated with both Glucobay and Calcipoheal-Cort combined. Haematoxylin & Eosin stain and S100 immunohistochemical staining were performed along with electron microscopic study of skin sections. Mean epidermal thickness and mean number of S100 immuno-positive keratinocytes were measured and measurements were statistically analyzed. Results: Group II mice showed psoriasis-like signs of skin inflammation. Groups III and IV mice showed less signs of inflammation which were markedly attenuated by combination of both of the treatments. Group II demonstrated significant acanthosis and abundant infiltrates of inflammatory cells in the dermis and significantly numerous S100 immuno-positive keratinocytes. Groups III and IV showed significant improvement of these changes which were markedly diminished in group V as it showed almost normal histological structure. Conclusion: Acarbose had an overall beneficial effect on psoriasis-mimicking mouse model triggered by IMQ, almost comparable to that demonstrated by calcipotriol/betamethasone. However, combination of both treatments exerted a more powerful therapeutic effect.