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Showing 2 results for Hyperglycemia
Zeynab Rezaei, Zahra Abedi Kichi, Mehrdad Behmanesh,
Volume 11, Issue 2 (6-2020)
Abstract
Abstract: Hyperglycemia is a major cause of diabetes. Hyperglycemia-induced endothelial dysfunction is generally believed to be the basis of diabetic vascular complications such as retinopathy, nephropathy and cardiovascular diseases. The most important molecules in endothelial cells that can sense elevated level of glucose and transmit signals into the cell are G protein-coupled receptors (GPCRs).
In the present study, according to bioinformatics analysis of genomic sequences between healthy and patient individuals, two G proteins GPR182 and CALCRL were selected and their expression level were examined in hyperglycemic and normal conditions in HUVEC as a model of vascular endothelial cells at different glucose concentrations and various time intervals. In addition, the effects of hyperglycemia on cell viability and cell cytotoxicity were assessed by MTT and LDH assay respectively and also morphological changes by immunohistochemistry.
Overall our data reveal a probable role for GPR182 and CALCRL in hyperglycemia-induced endothelial dysfunction. Thus, they could be developed as a potential molecular targets for the endothelial dysfunction therapy.
Volume 26, Issue 3 (9-2023)
Abstract
Introduction: The antioxidant enzymes and antioxidant capacity are affected by hyperglycemia in the different tissues of human body during diabetes mellitus (DM). Hence, in the present study we measured the activity of catalase and glutathione content in the livers of streptozotocin-induced diabetic rats.
Methods: Male Wistar rats were randomly divided into normal and diabetic groups (n=6). To induce DM, a single intravenous injection of streptozotocin was used (45 mg/kg). Blood glucose of rats was measured at the beginning and termination of study. Likewise, the activity of catalase and the content of glutathione were determined in the livers at termination of the study.
Results: Induction of DM increased blood glucose of the diabetic rats to 559 ± 35 mg/dL. This value did not change during the test (610 ± 17 mg/dL) in diabetic rats. Diabetes also increased the catalase activity in the livers of diabetic rats compared to normal group. Likewise, glutathione content increased in the livers of diabetic animals compared to normal rats.
Conclusion: Our findings revealed that the activity of antioxidant enzymes as well as antioxidant capacity of liver may be increased as a compensatory response to confront the tissue oxidative stress for the determined time during diabetes. It is suggested, if the period of diabetes be prolonged, this compensatory response may be weakened.
