Objectives: The aim of the study was to determine the relationships between microRNA-20a and microRNA-125b expression and apoptosis and inflammation in a rat model of spinal cord injury (SCI) using microscopy, immunohistochemistry, and molecular biology. Methods: Sixty-one rats were divided into three groups: a control group that was not subjected to any operation; a sham-operated group; and an experimental group that was subjected to spinal cord compression. The experimental group was further subdivided into two subgroups: the experimental control group, which did not receive any drug treatment; and the methylprednisolone treatment group, which received 30 mg/kg methylprednisolone on day 0 followed by 10 mg/kg/day methylprednisolone from days 1–14. Results: Tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 levels increased in the experimental control group on days 1 and 3, and decreased in the experimental control group and methylprednisolone treatment group on days 7 and 14. Caspase-3 levels increased in the experimental control group on day 1, and decreased in the experimental control group and methylprednisolone treatment group on days 3, 7, and 14. MicroRNA-20a expression was upregulated in the experimental control group on days 1 and 3, and microRNA-125b expression was downregulated on days 3 and 7. Conclusions: After SCI, upregulated microRNA-20a expression and increased proinflammatory cytokines may lead to an increase in inflammation. MicroRNA-125b may be associated with caspase-3, and microRNA-125b downregulation may inhibit apoptosis. Although the results of this study suggest potential relationships between microRNA-20a and microRNA-125b expression and apoptosis and inflammation in SCI, further studies are needed to confirm microRNA-20a and microRNA-125b as biomarkers in SCI and to develop new strategies for the treatment of SCI.
19 March 2022 in Biochemical and Biophysical Research Communications
Aim: Adolescents are at risk due to the intensive use of mobile phones. The aim of this study was to investigate the histopathological and biochemical effects of 900-Megahertz electromagnetic field on spleen in late adolescent period, exposed during periods of early and mid-adolescence.Material and Methods: In this study, 24 Sprague Dawley 21-day-old male rats were divided into control (n=8), sham (n=8) and electromagnetic field groups (n=8). Control group rats were not subjected to any application. Electromagnetic field group rats were taken into the electromagnetic field cage and were exposed to 900-Megahertz electromagnetic field (1 hour per day for 25 days). Sham group rats were taken into the electromagnetic field cages but were not exposed to electromagnetic field. At the end of the treatment, all animals were sacrificed by cervical dislocation method and the spleens were removed. After histological procedures, tissue sections were taken and stained with hematoxylin-eosin and periodic acid Schiff. Histopathological evaluation was performed on the spleen tissues. Oxidative stress parameters including lipid peroxidation, superoxide dismutase, glutathione and catalase levels were investigated via biochemical analysis.Results: Histopathological evaluation revealed megakaryocyte cells, enlarged white pulps and dilated sinusoids in spleen tissues of adolescent rats in electromagnetic field group. According to biochemical analysis results, it was determined that glutathione and lipid peroxidation values were increased, but superoxide dismutase and catalase values were decreased.Conclusion: It can be said that the 900-Megahertz electromagnetic field applied in adolescent period caused morphological changes on spleen tissue and caused oxidative stress in male rats.