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During the coronavirus disease 2019 (COVID-19) pandemic, cognitive impairment of varying degrees of severity began to be observed in a significant percentage of patients. The present study discussed the impact of immunological processes on structural and functional changes in the central nervous system and the related cognitive disorders. The purpose of the present review was to analyse and discuss available information from the scientific literature considering the possible relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infection and cognitive impairment, including NeuroCOVID, frontal syndrome and cytokine storm. A systematic literature review was conducted using: Google Scholar, Elsevier and the PubMed database. When searching for materials, the following keywords were used: 'cognitive dysfunctions', 'SARS-CoV-2', 'COVID-19', 'Neuro-SARS2', 'NeuroCOVID', 'frontal syndrome', 'cytokine storm', 'Long COVID-19'. A total of 96 articles were included in the study. The analysis focused on the characteristics of each study's materials, methods, results and conclusions. SARS-CoV-2 infection may induce or influence existing cognitive disorders of various nature and severity. The influence of immunological factors related to the response against SARS-CoV-2 on the disturbance of cerebral perfusion, the functioning of nerve cells and the neuroprotective effect has been demonstrated. Particular importance is attached to the cytokine storm and the related difference between pro- and anti-inflammatory effects, oxidative stress, disturbances in the regulation of the hypothalamic-pituitary-adrenal axis and the stress response of the body. [ABSTRACT FROM AUTHOR]

The treatment of diabetes and its complications is a key challenge for healthcare professionals. Accelerated atherosclerosis is associated with progressive diabetes, and it has been indicated that macrophages serve a crucial function in this process. Currently, the first-line treatment of diabetes is based on metformin, which is an inducer of AMP-activated protein kinase (AMPK) and belongs to the biguanide class of pharmaceuticals. It has been previously demonstrated that metformin exhibits more than just hypoglycemic effects. Therefore, the aim of the present study was to investigate the in vitro impact of metformin on cell viability and the expression levels of nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase (p22phox), a major enzyme in reactive oxygen species generation, and the three antioxidative enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) in monocytes/macrophages derived from 10 healthy volunteers. The effects of metformin were observed in the presence or absence of lipopolysaccharide (LPS), which was administered to induce oxidative stress. Furthermore, certain cells were treated with compound C, an inhibitor of AMPK, in order to determine the mechanistic role played by AMPK in the oxidative changes in the macrophages. Cell viability was evaluated using trypan blue and MTT assays. The mRNA and protein expression levels of p22phox and the various antioxidative enzymes were determined using polymerase chain reaction and western blot analysis, respectively. The results indicated that metformin, predominantly in LPS-pretreated monocytes/macrophages, reduced the expression levels of p22phox and increased those of SOD and GPx, but had only a minor effect on CAT levels. Therefore, metformin appears to alter the oxidative status of macrophages toward increasingly antioxidative activity, which may account for the pleiotropic effects observed during metformin treatment. [ABSTRACT FROM AUTHOR]

Obesity is associated with an increased risk of certain types of cancer, including colon cancer. Adipose tissue is an endocrine organ that produces biologically active substances, such as leptin and ghrelin. Recent research has suggested that adipose-derived hormones may be associated with mechanisms linked to tumorigenesis and cancer progression. Furthermore, previous studies have demonstrated that pineal gland-derived melatonin possesses important oncostatic and antioxidant properties. The present study aimed to determine the effects of the adipokines ghrelin and leptin, and the melatonin on intracellular levels of reactive oxygen species (ROS) and the activity of selected antioxidant enzymes, such as superoxide dismutase, catalase (CAT) and glutathione peroxidase. The effects of these compounds were also determined on the viability of HCT 116 human colorectal carcinoma cells in vitro. The pro-oxidant and growth inhibitory effects of melatonin resulted in an accumulation of ROS and decreased antioxidant capacity in melatonin-treated cells. Ghrelin administration alone caused a significant decrease in the levels of ROS, due to an increased activity of CAT in the HCT 116 cells. In addition, the present study observed increased lipid peroxidation following melatonin treatment, and decreased levels of malondialdehyde following ghrelin or leptin treatment. In conclusion, ghrelin, leptin and melatonin have various influences on the antioxidant capacity of HCT 116 cells. Compared with the adipokines, treatment with melatonin increased ROS levels and decreased cellular viability. [ABSTRACT FROM AUTHOR]