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INTRODUCTION: Diabetes is a chronic and progressive disease that usually causes disrupts the function of the body's organs and can eventually lead to cardiomyopathy, nephropathy, retinopathy, and neuropathy. Diabetic nephropathy (DN) is the most common cause of chronic kidney disease and causes chronic structural changes in different parts of the affected kidney. Glycocalyx layer is one of the most important components of the vascular base found in the endothelium throughout the body's arteries and it has been shown that glycocalyx is also damaged during diabetic nephropathy. Our goal is to conduct this systematic review study is to find the cause-and-effect relationship between glycocalyx and diabetic nephropathy and also to clarify the role of the endothelial renal glycocalyx in understanding of mechanism of the course of diabetic nephropathy, and to provide an accurate background for further important studies. METHODS: All databases included MEDLINE (PubMed), Science Direct, Scopus, Ovid and Google Scholar were systematically searched for related published articles. In all databases, the following search strategy was implemented and these key words (in the title/abstract) were used: "diabetes" AND "glycocalyx" OR "diabetic nephropathy" AND "glycocalyx". RESULTS AND DISCUSSION: A total of 19 articles were retrieved from all databases using search strategy. After screening based on the title and abstract, number of 17 of them selected for full text assessment. Finally, after extracting the key points and making connections between the articles, we came up with new points to consider. It can be said that diabetes with the action of reactive oxygen species through oxidative stress, increases ICAM-1 and TNF-α and decreases heparanase enzyme, it affects the glomerular endothelium and eventually leads to albuminuria and destruction of the Glx layer. CONCLUSION: Diabetes causes super-structural changes in the kidney nephrons at the glomerular level. The glomerular filter barrier, which includes the epithelial cell called the podocyte, endothelial pore cells, and basal membrane of the glomerulus, plays a major role in stabilizing the selective glomerular function in healthy individuals. Diabetic nephropathy also causes changes in endothelial glycocalyx.
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Learning and memory deficits appear in chronic diabetes and valproic acid has been proved to be beneficial in neurodegenerative diseases. Hence, the current study investigated the effectiveness of chronic valproate treatment for diabetes-induced memory impairment and increased levels of hippocampal apoptotic caspases. This study was conducted in adult male C57B15/J mice. Diabetes, which was induced by alloxan (150 mg/kg; i.p.), was confirmed when fasting blood sugar (FBS) was > 200 mg/dl. Sodium valproate (100 mg/kg; i.p.) was administrated to the diabetic and non-diabetic groups, every 72 h for 2 months. Next, all groups were evaluated for memory performance using the radial maze and shuttle box. After FBS measurement, animals were killed and the hippocampus was extracted and prepared for ELISA to assess caspase levels. Diabetic animals had significantly high FBS and memory impairment 2 months after the alloxan injection. Hippocampal levels of caspases 3, 6, and 8 were significantly higher in the diabetic group than in the control group. However, valproate treatment of diabetic animals significantly improved memory performance in both the radial maze and shuttle box and reduced the elevated levels of hippocampal apoptotic caspases, in comparison with diabetic animals. Chronic administration of valproate seems to have beneficial effects on diabetic neuropathy.