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4 result(s) for "Elberry, Dalia Azmy"
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Amelioration of gut dysbiosis-induced cognitive deterioration by repeated administration of human clostridium butyricum: targeting intestinal and blood–brain barrier
Background Disturbed intestinal integrity and increased permeability are linked to dysbiosis. This disruption involves GIT-related and unrelated diseases, such as neurological diseases. Intake of a high-fat diet (HFD) leads to an imbalance of gut microbiota and regression of bacteria producing “short-chain fatty acids (SCFAs)”. These SCFAs can modulate brain functions. Therefore, we investigated the therapeutic effect of Clostridium Butyricum (CB) bacteria extracted from human faeces on intestinal and neurological impairments induced by HFD and explored their modulation of tight junction protein expression. Materials and methods Twenty-four adult male rats were classified into the control group, which received regular rat chow; the HFD group, which received HFD for 16 weeks; and the HFD-Microbiota group, which received HFD as in group II for 16 weeks, but from week 9 received CB (dose of 2 ml (2.3 × 10 11  cfu/ml) daily till scarification. Results The microbiota improved working memory, episodic-like memory, and emotional memory. Also, there was a substantial decline in the animals’ body weights, serum lipopolysaccharides, interleukin-1β, tumour necrosis factor-α, insulin, glucose, and HOMA index compared to the HFD group. A remarkable increase in brain and colonic claudin-5 and occluding expression of its gene in the microbiota-treated group in comparison with the HFD group was reported. SCFAs, intestinal, brain claudin-5, and occludin genes were positively correlated. Also, a positive correlation was found between the F/B ratio and both brain beta-amyloid and Tau proteins. Conclusion Repeated intake of CB hindered systemic /neuroinflammation, enhanced the tight junction proteins’ expression in the gut/brain barrier, and improved cognitive functions.
Effect of Allopregnanolone on Spatial Memory and Synaptic Proteins in Animal Model of Metabolic Syndrome
Metabolic Syndrome (MetS) is considered a common disorder, especially with a sedentary lifestyle and unhealthy food consumption. Cognitive impairment is one of the MetS consequences that worsens the quality of life of the patients. The study aimed to assess the therapeutic effect of the neurosteroid Allopregnalonone on spatial memory and, therefore, the expression of two synaptic plasticity markers in the hippocampus. Thirty-two male rats were divided into four groups: control groups, MetS, and MetS + Allopregnalone. Spatial memory has been evaluated by the Y-maze task and blood pressure measured by the rat tail method. Biochemical evaluation of serum glucose, insulin, lipid profile, and hippocampal expression of Synaptophysin and Associated Protein 43 (GAP-43) were performed for assessing Allopregnanolone on serum and hippocampal markers. Allopregnanolone therapy improved working spatial memory, hypertension, and biochemical markers measured in the serum and hippocampus.
Effect of undifferentiated versus hepatogenic partially differentiated mesenchymal stem cells on hepatic and cognitive functions in liver cirrhosis
Liver cirrhosis is the outcome of chronic liver injury. The current study aimed to investigate the therapeutic effect of undifferentiated mesenchymal stem cells versus partially differentiated mesenchymal stem cells on liver cirrhosis and hepatic encephalopathy. 50 adult male albino rats constituted the animal model and were divided into the following groups: control, thioacetamide, undifferentiated mesenchymal stem cells and hepatocyte growth factor-differentiated mesenchymal stem cells groups. Cognitive assessment was achieved by open field test and Y-maze task. We measured serum alanine aminotransferase, albumin and transforming growth factor-beta1, gene expression of α-smooth muscle actin, matrix metalloprotein-2, its tissue inhibitor and apoptotic markers: Bax and Bcl2, brain glial fibrillary acidic protein, synaptophysin, and dopaminergic receptors.
Comparing the Effect of Heat Therapy and Mitochondrial-Targeted Antioxidants in Polycystic Ovarian Syndrome Phenotype Induced by Junk Food Consumption
Polycystic ovarian syndrome (PCOS) is a complex endocrine-metabolic disorder, and multiple factors contribute to its pathophysiology. The current study assessed a PCOS-like animal model induced by consuming a high-fat sugar (HFHS) diet and compared the treatment outcome of mitochondrial-targeted antioxidants versus heat therapy. Sixty rats were divided into the following study groups: three control groups (negative and positive for the treatments used), HFHS, hot tub therapy (HTT) treatment, and MitoQ10 treatment (500 µmol/L MitoQ10 in clean drinking water daily, from week fourteen till week twenty-two of the study). At week fourteen, PCOS was confirmed by vaginal smear examination; measurements of blood testosterone (T), anti-Mullerian hormone (AMH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), glucose, and insulin; and determination of the homeostatic model assessment of IR (HOMA-IR). At week 22, blood samples were collected for measurement of the serum LH, FSH, AMH, T, insulin, glucose, lipid profile, kisspeptin, ADAM metallopeptidase with thrombospondin type 1 motif 19 (ADAMTS19), S100 calcium-binding protein B (S100B), fibulin 1 (FBLN1), immunoglobulin free light chains (FLCs), kappa and lambda. Ovaries were examined for morphological changes; for the levels of glutathione (GSH), catalase, SOD, malondialdehyde (MDA), and nitric oxide (NO); and the expression of FK506 binding protein 52 (FKBP52) and the androgen receptor (AR). The consumption of HFHS diet-induced PCOS-like features, which have been ameliorated by both HTT and mitoQ10 as potential therapies, with MitoQ10 showing a superior effect over HTT. Graphical Abstract