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1.
Curr Med Chem ; 29(11): 1920-1935, 2022.
Article in English | MEDLINE | ID: mdl-34375177

ABSTRACT

Diabetes mellitus (DM) and DM-induced vascular complications are significant global healthcare problems, causing a decrease in patient quality of life. The main reason for the disability and mortality of patients is rapidly progressing micro-and macroangiopathies. Currently, free radical oxidation is recognized as one of the main mechanisms in the development of DM and associated complications. Under normal physiological conditions, the level of free radicals and antioxidant defense capabilities is balanced. However, imbalance occurs between the antioxidant defense system and pro-oxidants during chronic hyperglycemia and may invoke the formation of excess free radicals, leading to activation of lipid peroxidation and accumulation of highly toxic products of free radical oxidation. This is accompanied by varying degrees of insulin deficiency and insulin resistance in DM patients. Simultaneously with the activation of free radical generation, a decrease in the activity of antioxidant defense factors (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, vitamins C and E) and an acceleration of diabetic complications are seen. Therefore, we hypothesize that antioxidants may play a positive role in the treatment of DM patients to prevent DM-induced vascular complications. However, this has not been sufficiently studied. In this review, we discuss recent insights into the potential underlying mechanisms of oxidative stress-induced diabetic complications and the implications of antioxidants in mitigation of DM-induced vascular complications.


Subject(s)
Diabetes Complications , Diabetes Mellitus , Antioxidants/pharmacology , Diabetes Complications/drug therapy , Diabetes Complications/prevention & control , Diabetes Mellitus/drug therapy , Free Radicals , Glutathione Peroxidase/metabolism , Humans , Lipid Peroxidation , Oxidative Stress , Quality of Life , Superoxide Dismutase/metabolism
2.
Curr Neuropharmacol ; 20(3): 630-647, 2022 Mar 04.
Article in English | MEDLINE | ID: mdl-34365923

ABSTRACT

BACKGROUND: Stroke is a major challenge in neurology due to its multifactorial genesis and irreversible consequences. Processes of endogenous post-stroke neurogenesis, although insufficient, may indicate possible direction of future therapy. Multiple research considers stem-cell-based approaches in order to maximize neuroregeneration and minimize post-stroke deficits. OBJECTIVE: Aim of this study is to review current literature considering post-stroke stem-cell- based therapy and possibilities of inducing neuroregeneration after brain vascular damage. METHODS: Papers included in this article were obtained from PubMed and MEDLINE databases. The following medical subject headings (MeSH) were used: "stem cell therapy", "post-stroke neurogenesis", "stem-cells stroke", "stroke neurogenesis", "stroke stem cells", "stroke", "cell therapy", "neuroregeneration", "neurogenesis", "stem-cell human", "cell therapy in human". Ultimate inclusion was made after manual review of the obtained reference list. RESULTS: Attempts of stimulating neuroregeneration after stroke found in current literature include supporting endogenous neurogenesis, different routes of exogenous stem cells supplying and extracellular vesicles used as a method of particle transport. CONCLUSION: Although further research in this field is required, post stroke brain recovery supported by exogenous stem cells seems to be promising future therapy revolutionizing modern neurology.


Subject(s)
Brain Ischemia , Stroke , Humans , Neurogenesis , Stem Cell Transplantation/methods , Stroke/therapy
3.
Mol Neurobiol ; 57(7): 3014-3026, 2020 Jul.
Article in English | MEDLINE | ID: mdl-32458388

ABSTRACT

Oxidative stress associated with chronic cerebral hypoperfusion is one of the fundamental factors leading to neurodegenerative diseases. To prevent oxidative stress, physical activity is effective. Physical exercise enables development of rehabilitation techniques that can progressively increase patients' stress resistance. We determined the oxidative stress dynamics in experimental hypoperfusion and modeled rehabilitation measures, comparing sex and stress resistance levels. The experiment was performed on 240 Wistar rats of both sexes over a period of 90 days. Based on behavioral test results obtained using the open field test, the rats were divided into active animals with predicted higher stress resistance (HSR) and passive animals with predicted lower stress resistance (LSR). TBA (thiobarbituric acid) plasma concentration of the active products (malondialdehyde-MDA), blood plasma (NO-X) concentration, and L-citrulline (LC) concentration were determined spectrophotometrically at the corresponding wave length (nm). The intensity of oxidative stress was evaluated using the chemoluminscent method to determine the blood plasma antioxidant activity on the BCL-07 biochemoluminometer. This study revealed two stages of oxidative stress: a less pronounced phase covering the first days after surgery and a main one, which starts from the month after the operation to 3 months. Female sex and a high initial level of stress resistance reduced the severity of oxidative stress. Physical activity commencing a week after the surgery resulted in "reloading" the adaptive mechanisms and slowed the onset of the main stage, leading to a decrease in the free-radical process in all studied subgroups and the greater blood plasma (NO)-X decrease in the male animals. Future neuropharmacological intervention most likely will be able to determine the pathophysiology mechanism of chronic brain hypoperfusion and potentially extending adaptive responses.


Subject(s)
Brain Ischemia/metabolism , Brain/metabolism , Oxidative Stress/physiology , Physical Conditioning, Animal/physiology , Stress, Psychological/metabolism , Animals , Female , Male , Malondialdehyde/blood , Maze Learning/physiology , Rats, Wistar , Sex Factors , Thiobarbiturates/blood
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