Bdnf impact on biological markers of depression—role of physical exercise and training

Depression is the most common and devastating psychiatric disorder in the world. Its symptoms, especially during the pandemic, are observed in all age groups. Exercise training (ET) is well known as a non-pharmacological strategy to alleviate clinical depression. The brain-derived neurotrophic factor (BDNF) is one of the biological factors whose expression and secretion are intensified in response to ET. BDNF is also secreted by contracted skeletal muscle that likely exerts para-, auto-and endocrine effects, supporting the crosstalk between skeletal muscle and other distant organs/tissues, such as the nervous system. This finding suggests that they communicate and work together to induce improvements on mood, cognition, and learning processes as BDNF is the main player in the neurogenesis, growth, and survival of neurons. Therefore, BDNF has been recognized as a therapeutic factor in clinical depression, especially in response to ET. The underlying mechanisms through which ET impacts depression are varied. The aim of this review was to provide information of the biological markers of depression such as monoamines, tryptophan, endocannabinoids, markers of inflammatory processes (oxidative stress and cytokines) stress and sex hormones and their relationship to BDNF. In addition, we reviewed the effects of ET on BNDF expression and how it impacts depression as well as the potential mechanisms mediating this process, providing a better understanding of underlying ET-related mechanisms in depression.Internal grant of University School of Physical Education. Project No. 503 62/05 Effectiveness of various therapeutic forms and their influence on nervous, muscular and vascular plasticity in patients after ischemic stroke”

Oxidative stress and S-100B protein in children with bacterial meningitis

<p>Abstract</p> <p>Background</p> <p>Bacterial meningitis is often associated with cerebral compromise which may be responsible for neurological sequelae in nearly half of the survivors. Little is known about the mechanisms of CNS involvement in bacterial meningitis. Several studies have provided substantial evidence for the key role of nitric oxide (NO) and reactive oxygen species in the complex pathophysiology of bacterial meningitis.</p> <p>Methods</p> <p>In the present study, serum and CSF levels of NO, lipid peroxide (LPO) (mediators for oxidative stress and lipid peroxidation); total thiol, superoxide dismutase (SOD) (antioxidant mediators) and S-100B protein (mediator of astrocytes activation and injury), were investigated in children with bacterial meningitis (n = 40). Albumin ratio (CSF/serum) is a marker of blood-CSF barriers integrity, while mediator index (mediator ratio/albumin ratio) is indicative of intrathecal synthesis.</p> <p>Results</p> <p>Compared to normal children (n = 20), patients had lower serum albumin but higher NO, LPO, total thiol, SOD and S-100B. The ratios and indices of NO and LPO indicate blood-CSF barriers dysfunction, while the ratio of S-100B indicates intrathecal synthesis. Changes were marked among patients with positive culture and those with neurological complications. Positive correlation was found between NO index with CSF WBCs (r = 0.319, p < 0.05); CSF-LPO with CSF-protein (r = 0.423, p < 0.01); total thiol with LPO indices (r = 0.725, p < 0.0001); S-100B and Pediatric Glasow Coma Scores (0.608, p < 0.0001); CSF-LPO with CSF-S-100B (r = 0.482, p < 0.002); serum-total thiol with serum S-100B (r = 0.423, p < 0.01).</p> <p>Conclusion</p> <p>This study suggests that loss of integrity of brain-CSF barriers, oxidative stress and S-100B may contribute to the severity and neurological complications of bacterial meningitis.</p

Effects of adaptive exercise on apoptosis in cells of rat renal tubuli.

Eur J Appl Physiol. 2007 Feb;99(3):217-26. Epub 2006 Nov 11. Effects of adaptive exercise on apoptosis in cells of rat renal tubuli. Podhorska-Okolow M, Dziegiel P, Murawska-Cialowicz E, Saczko J, Kulbacka J, Gomulkiewicz A, Rossini K, Jethon Z, Carraro U, Zabel M. Source Department of Histology and Embryology, Medical University of Wroclaw, Wroclaw, Poland. [email protected] Abstract Regular exercise is known to improve physiological and functional capacity of many organs due to adaptive processes. We have previously shown that acute exercise in untrained rats results in apoptosis of renal tubular cells and that the apoptotic process seems to be associated with stimulation of angiotensin II, AT1 and AT2 receptors. In this study, we examined the influence of regular training on apoptosis and the role of angiotensin II receptors and antioxidant enzymes in mediating the adaptive response in renal tubular cells. We measured apoptosis, expression of AT1 and AT2 receptors, level of lipid peroxidation (TBARS) and activities of antioxidant enzymes, SOD, GPx and CAT in kidneys of sedentary rats that were exposed to acute exercise and rats that were trained for 8 weeks. In untrained animals, the acute exercise resulted in increased apoptosis and increased expression of AT1 and AT2 receptors in renal tubular cells, while in the rats exposed to the 8-week regular training, there were no changes in apoptosis nor AT1 and AT2 receptor expression as compared to the sedentary animals. The TBARS levels were significantly increased in acutely exercised rats, while in rats pre-exposed to the training they remained unchanged. The acute exercise, as well as regular training, did not change SOD, CAT or GPx activities. These findings suggested that the acute exercise-induced apoptosis in renal tubules could involve action of AT1 and AT2 receptors as well as oxidative stress, while the regular training was shown to prevent apoptosis in renal tubular cells via modulated expression of AT1 and AT2 receptors. PMID: 17102979 [PubMed - indexed for MEDLINE