Effects Of Chronic Stress Research Articles

Effects of chronic empathic stress on synaptic efficacy, as well as short-term and long-term plasticity at the Schaffer collateral/commissural- CA1 synapses in the dorsal hippocampus of rats.

Empathy, the ability to comprehend and share others' emotional states, impacts brain functions. This invivo electrophysiological study explored the influence of chronic empathic stress on synaptic efficacy, as well as short-term and long-term plasticity at the Schaffer collateral/Commissural - CA1 synapses in the dorsal hippocampus of rats, in situations of social equality and inequality. Forty-eight male rats were randomized into six groups: control, pseudo-observer, pseudo-demonstrator, observer, demonstrator, and co-demonstrator(Co, Pse-Ob, Pse-De, Ob, De, Co-De) groups. Stress induction(2h/day, 21 days) was performed in situations of equality and inequality. Serum corticosterone levels, slope, amplitude, and area under the curve(AUC) of field excitatory postsynaptic potentials(fEPSPs) were assessed in the hippocampal CA1 area using input-output(I/O) functions, paired-pulse(PP) responses with different interpulse intervals(IPIs), and long-term potentiation (LTP) after high-frequency stimulation (HFS). The fEPSP slope, amplitude, and AUC significantly decreased in all stress groups, especially in the De and Pse-De groups. These parameters were significantly increased in the Co-De and Ob groups compared to theDe group. Notably, the corticosterone levels strongly confirmed the electrophysiological findings. Chronic empathic stress could disrupt synaptic efficacy and plasticity in the CA1 area. Empathic stress, involving the presence of cagemates in situations of social equality and inequality, can modify long-term plasticity and serum corticosterone levels in demonstrators and co-demonstrators. Under empathic stress related to situations of inequality, freely moving observers may influence the demonstrators' stress experience. Therefore, the presence of a conspecific in the social inequality conditions had significant suppressive effects on long-term plasticity, while conversely, under equality conditions, long-term plasticity was favorably improved through social buffering.

Tinjauan Literatur Sistematis: Hubungan antara Technostress dengan Burnout

This systematic literature review investigates the relationship between technostress and burnout in various organizational and educational contexts. Technostress arises from excessive or imbalanced use of information technology in work or learning environments, which can adversely affect individuals' psychological well-being. Burnout, on the other hand, is a consequence of chronic stress experienced in work or educational settings. The study involves systematic steps in searching, selecting, evaluating, and synthesizing relevant literature from academic databases and other sources. Findings from the literature review reveal that technostress factors such as techno-overload, techno-invasion, techno-complexity, and others significantly contribute to individuals' levels of burnout. Recommendations for future research include the need for a mixed methods approach integrating quantitative and qualitative methods to gain deeper understanding, as well as longitudinal studies to track the development of technostress and burnout over time. This research provides a strong foundation for the development of effective policies and management practices aimed at reducing the negative impacts of technostress and enhancing individual well-being in modern work and educational environments.

Effects of chronic cold stress and thermal stress on growth performance, hepatic apoptosis, oxidative stress, immune response and gut microbiota of juvenile hybrid sturgeon (Acipenser baerii ♀ × A. schrenkii ♂)

The current study was conducted to investigate the effects of chronic cold stress and thermal stress on the growth performance, hepatic oxidative status, immune response, apoptosis and gut microbiota in juvenile hybrid sturgeon. The fish (initial mean weight: 21.4 ± 0.3 g) was reared at three temperatures (14 °C, 22 °C, and 30 °C) for 16 d, which were termed as low temperature group (LT), moderate temperature group (MT), and high temperature group (HT), respectively, and the second group was regarded as control group in this study. Each group was assigned randomly to three tanks with 15 fish per replica. The results indicated that cold stress resulted in a significant reduction of growth metrics and a significant increase of feed conversion ratio in fish compared with MT group. Interestingly, cold stress increased hepatocyte apoptosis revealed by TUNEL staining, along with nuclear disappearance in H&E-stained sections and elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Transcriptional levels of apoptosis-related genes and toll-like receptor signaling pathway components were significantly up-regulated in liver under cold stress. Compared with control group, in terms of thermal stress, the growth performance and feed utilization of fish were declined to some extent compared with MT group. Moreover, high temperature significantly elevated hepatic productions of malondialdehyde and hydrogen peroxide, as well as increased activities of some antioxidant enzymes in liver. In addition, low and high temperature induce changes in the composition of gut microbiota. Overall, the results suggested that cold stress decelerated growth performance, induced hepatocyte apoptosis, and enhanced innate immunity in hybrid sturgeon to cope with additional stressors. Whereas, thermal stress resulted in hepatic oxidative stress in liver and the protective responses in the antioxidant enzymes in fish were activated. These results provided insights into the different physiological adaptation strategies in responsive to cold stress and thermal stress in this cold-water fish.

The West: An autoimmune disease?

ContextThis work explores the paradoxical stress mechanisms in Western societies, marked by consumption and comfort. Despite the perceived well-being of modern capitalist societies, a profound psychosomatic discontent manifests, reflected in the rise of stress-induced illnesses, autoimmune diseases, and psychiatric disorders. The article uses the metaphor of autoimmunity to describe Western societal dysfunction, drawing parallels between biological self-destruction and societal self-harm driven by hyper-individualism, economic pressures, and digital dependencies. ObjectivesThis study aims to analyze the mechanisms through which Western societies contribute to self-destructive processes, paralleling the way autoimmune diseases function within the body. It seeks to demonstrate how excessive control, consumerism, and the digital environment exacerbate stress, which in turn contributes to both physical and psychological deterioration. The philosophical question underpinning this analysis is whether the societal and economic systems in the West are undermining the self-defense mechanisms of their members, akin to an autoimmune response. MethodThe article adopts a qualitative and theoretical approach, integrating concepts from psychology, psychoneuroimmunology, and epidemiology. The author incorporates clinical observations, epidemiological data, and philosophical reflections to explore the effects of chronic stress on mental and physical health. Drawing on psychoneuroimmunology, the research explores the bi-directional interaction between the mind, nervous system, and immune function, focusing on the relationship between stress, inflammation and autoimmune diseases. ResultsOur exploration reveals a significant correlation between the rise of autoimmune diseases and the psychosocial stresses of Western capitalist societies. Epidemiological data support the link between chronic stress, psychiatric disorders, and autoimmune conditions. The article also highlights how the digital economy's manipulation of stress and fear (such as through FOMO) contributes to widespread psychological distress. This stress, in turn, disrupts immune function, leading to a cycle of physical and psychological degeneration. InterpretationWestern societies, through their relentless pursuit of control, comfort, and consumption, create environments of heightened stress that mirror the dysfunctions of autoimmune diseases, where the body turns against itself. The research suggests that modern capitalist structures are pathogenic, exacerbating stress, weakening immune resilience, and fostering mental health crises. The article concludes that a holistic approach is necessary to address this systemic dysfunction, advocating for a reconceptualization of health that integrates mental, physical, and societal well-being.

Reproductive effects of wartime stress and possibilities of their correction (Literature review)

The article presents modern literary data and data of own clinical observations regarding the effects of long-term chronic stress on reproductive processes with an emphasis on the effects of wartime. All stages of the reproductive cycle, from the regulation of the menstrual cycle, conception and implantation to the birth of a child, are energy-consuming and unprofitable for the body. All these processes require a lot of energy, but their purpose is to reproduce the species, not to maintain homeostasis. Therefore, the body temporarily slows down these processes, withdraws energy aimed at their support, and uses it to resist stress.The biological meaning of inhibition of reproductive function in stressful conditions is that if a woman becomes pregnant under unfavorable conditions, it is bad for her body, and for the offspring, and for the future prospects of the biological species as a whole. Therefore, from an evolutionary point of view, it is very beneficial to reduce the production of hormones, exclude ovulation and prevent implantation, and reduce libido during periods of high stress.Stress causes activation of the neuroendocrine and sympatho-adrenal systems, which leads to the release of such hormones as cortisol, adrenaline, norepinephrine into the blood. This helps to mobilize the body’s resources to overcome a threatening situation. However, prolonged stress depletes these systems and leads to maladjustment and increased risk of disease. Stress hormones affect all body systems, including the reproductive system. According to the literature, stress disorders occur three times more often in women than in men.In conditions of chronic stress, in particular during war, pregnancy complications can be caused by stress of various origins: metabolic, associated with micronutrient deficiency, psychological, physical, a combination of factors.Prenatal stress during wartime is a part of our existence, which reduces the quality of life of a pregnant woman and affects the intrauterine development of the fetus and the subsequent health of the child. Long-term chronic stress also leads to deterioration of the general state of health of the expectant mother: it reduces work capacity and appetite, causes lethargy, apathy, sleep disturbances, and increases the risk of obstetric complications.Stress negatively affects the state of immunity of the female population both before conception and during pregnancy, which can lead to the activation of latent infections, and makes the body of pregnant women more vulnerable to acute seasonal infections. This is also facilitated by the lack of necessary vitamins and trace elements with antioxidant properties in conditions of occupation, disruptions in the supply of medicines to certain problematic regions of the country, frequent changes of residence, etc.During pregnancy, all the negative effects of wartime can be realized in the form of major obstetric syndromes. In conditions of pronounced energy deficit caused by long-term stress, the body has to provide for itself to the detriment of the future child, which leads to ZRP, and in the most tragic cases – to intrauterine death. Violation of the psycho-emotional state of pregnant women today leads to the birth of “children of war” – insecure, low self-esteem, deeply ill babies with mental disorders.For the onset of pregnancy and its successful bearing, vitamins and micro/macroelements with antioxidant properties are needed in order to resist oxidant stress inherent in stressful conditions (vitamins of group B, vitamin D, iron, magnesium, omega-3 polyunsaturated fatty acids, L-arginine, L- carnitine). Rational management of pregnancy in today’s complex conditions should be complex and multi-vector. One of the promising directions in ensuring an uncomplicated course of pregnancy and successful perinatal outcomes is work with perinatal psychologists. At the same time, the use of additional psychosomatic effects of basic therapy should not be underestimated.

Common biological processes and mutual crosstalk mechanisms between cardiovascular disease and cancer.

Cancer and cardiovascular disease (CVD) are leading causes of mortality and thus represent major health challenges worldwide. Clinical data suggest that cancer patients have an increased likelihood of developing cardiovascular disease, while epidemiologic studies have shown that patients with cardiovascular disease are also more likely to develop cancer. These observations underscore the increasing importance of studies exploring the mechanisms underlying the interaction between the two diseases. We review their common physiological processes and potential pathophysiological links. We explore the effects of chronic inflammation, oxidative stress, and disorders of fatty acid metabolism in CVD and cancer, and also provide insights into how cancer and its treatments affect heart health, as well as present recent advances in reverse cardio-oncology using a new classification approach.

EXPRESS: The effect of chronic academic stress on attentional bias towards value-associated stimuli.

Individuals typically exhibit attentional bias towards stimuli that are considered valuable. This study aimed to investigate the effect of chronic academic stress on attentional bias towards value-associated stimuli. Both the stress group (preparation for a critical academic examination) and the control group performed a modified dot-probe task. Two color stimuli were presented simultaneously, one of which was associated with high or low monetary rewards through the value-associated training. The participants were then instructed to respond to the location of a probe dot which was presented either congruent or incongruent towards the value-associated stimuli. In the neutral condition, both stimuli were not value-associated ones. The results showed that, 1) In the value-associated training task, shorter reaction times (RTs) and higher accuracies were observed for the high-value trials compared to the low-value trials in both groups, suggesting a successful association between neutral stimuli and value. 2) In the dot-probe task, the RTs were shorter for the high/low-value congruent conditions compared to the high/low-value incongruent conditions in both groups, suggesting an attentional bias towards value-associated stimuli. 3) Compared to the control group, the stress group showed an increased disengagement (RTincongruent - RTneutral) effect but a similar orienting (RTneutral - RTcongruent) effect. These results suggested that chronic academic stress may promote attentional bias towards value-associated stimuli by impairing attentional disengagement.

Sex-specific GABAergic microcircuits that switch vulnerability into resilience to stress and reverse the effects of chronic stress exposure.

Clinical and preclinical studies have identified somatostatin (SST)-positive interneurons as critical elements that regulate the vulnerability to stress-related psychiatric disorders. Conversely, disinhibition of SST neurons in mice results in resilience to the behavioral effects of chronic stress. Here, we established a low-dose chronic chemogenetic protocol to map these changes in positively and negatively motivated behaviors to specific brain regions. AAV-hM3Dq-mediated chronic activation of SST neurons in the prelimbic cortex (PLC) had antidepressant drug-like effects on anxiety- and anhedonia-like motivated behaviors in male but not female mice. Analogous manipulation of the ventral hippocampus (vHPC) had such effects in female but not male mice. Moreover, the activation of SST neurons in the PLC of male mice and the vHPC of female mice resulted in stress resilience. Activation of SST neurons in the PLC reversed prior chronic stress-induced defects in motivated behavior in males but was ineffective in females. Conversely, activation of SST neurons in the vHPC reversed chronic stress-induced behavioral alterations in females but not males. Quantitation of c-Fos+ and FosB+ neurons in chronic stress-exposed mice revealed that chronic activation of SST neurons leads to a paradoxical increase in pyramidal cell activity. Collectively, these data demonstrate that GABAergic microcircuits driven by dendrite targeting interneurons enable sex- and brain-region-specific neural plasticity that promotes stress resilience and reverses stress-induced anxiety- and anhedonia-like motivated behavior. The data provide a rationale for the lack of antidepressant efficacy of benzodiazepines and superior efficacy of dendrite-targeting, low-potency GABAA receptor agonists, independent of sex and despite striking sex differences in the relevant brain substrates.

Chronic social stress induces p16-mediated senescent cell accumulation in mice.

Life stress can shorten lifespan and increase risk for aging-related diseases, but the biology underlying this phenomenon remains unclear. Here we assessed the effect of chronic stress on cellular senescence-a hallmark of aging. Exposure to restraint stress, a psychological non-social stress model, increased p21Cip1 exclusively in the brains of male, but not female mice, and in a p16Ink4a-independent manner. Conversely, exposure to chronic subordination stress (only males were tested) increased key senescent cell markers in peripheral blood mononuclear cells, adipose tissue and brain, in a p16Ink4a-dependent manner. p16Ink4a-positive cells in the brain of chronic subordination stress-exposed mice were primarily hippocampal and cortical neurons with evidence of DNA damage that could be reduced by p16Ink4a cell clearance. Clearance of p16Ink4a-positive cells was not sufficient to ameliorate the adverse effects of social stress on measured metrics of healthspan. Overall, our findings indicate that social stress induces an organ-specific and p16Ink4a-dependent accumulation of senescent cells, illuminating a fundamental way by which the social environment can contribute to aging.

Time-limited access to palatable food reveals differential effects of psychological stress on homeostatic vs. hedonic feeding behavior in male rats

Psychological stress has complex effects on eating behavior, appearing to reduce homeostatically regulated feeding, while increasing hedonically motivated feeding. The present work tests this idea using two feeding paradigms that offer a highly palatable food on a time-limited basis, together with continual access to a low palatability food. This approach provides a natural separation between periods of eating that are primarily homeostatic vs. hedonically regulated. First, the impact of acute stress exposure on feeding behavior was tested using an acute “meal-dessert” paradigm. When fasted adult male rats were given a recent stressor of moderate intensity (restraint), refeeding with a chow-meal was reduced, without affecting chocolate-dessert intake, thereby increasing the proportion of calories derived from chocolate. Next, the effect of chronic moderate stress was tested using a “binge” eating paradigm. Chow-fed rats were given unexpected (3d per week) vs. expected (7d per week) brief access to a highly palatable high-fat diet (HFD), and feeding behavior was compared to control groups that were maintained with continuous access to only chow or only HFD. Chronic stress reduced total caloric intake in all groups, including binge-like HFD intake. Binge-like HFD intake caused metabolic dysfunction (increased adiposity and impaired glucose homeostasis) to an extent beyond that predicted by total caloric intake or body weight gain. Finally, binge-like HFD intake shifted stress coping behavior from an active to a passive phenotype, particularly in rats receiving concurrent chronic stress, suggesting the possibility of increased risk for stress-related disorders, like depression, in individuals who binge eat during stress.

Plasma proteomic signature of chronic psychosocial stress in mice

Chronic stress significantly impacts both physical and mental wellbeing, increasing risk of cardiovascular disease, immune dysregulation, and psychiatric conditions such as depression and anxiety disorders. The plasma proteome is a valuable source of biomarkers of health and disease, but the limited number of studies exploring the potential of the plasma proteome as a biomarker for stress-related disorders underscores the importance of further investigation of the effects of chronic stress on the plasma proteome. The aim of this study was to examine the effect of a 5-week chronic psychosocial stress paradigm on the plasma proteome in mice and to determine if any affected proteins correlated with stress-induced changes in behaviour and physiology, and thus might represent biomarkers of negative impacts of chronic stress. Using LC-MS/MS proteomic analysis, 38 proteins in the mouse plasma proteome were identified to be affected by chronic psychosocial stress. Functional analysis revealed that these proteins clustered into biological functions including inflammatory response, regulation of the immune response, complement and coagulation cascades, lipid metabolic process, and high-density lipoprotein particles Correlation analyses of the identified proteins with stress-induced behavioural or physiological changes stress revealed significant correlations between stress-induced anxiety-like behaviour and Phosphatidylinositol-glycan-specific phospholipase D, Complement C2, Epidermal growth factor receptor, Prosaposin, Actin-related protein 2/3 complex subunit 1B, Maltase-glucoamylase, Mannosyl-oligosaccharide 1,2-alpha-mannosidase IA and Fibrinogen-like protein 1. Chronic psychosocial stress blunted acute stress-induced corticosterone release, and this correlated with abundance of Pyrethroid hydrolase Ces2a; N-fatty-acyl-amino acid synthase/hydrolase Pm20d1, Mannosyl-oligosaccharide 1,2-alpha-mannosidase IA, Alpha-2-macroglobulin-P and L-selectin. Finally, stress-induced reductions in both brown and epididymal fat correlated with Phosphatidylinositol-glycan-specific phospholipase D, Complement C2, Epidermal growth factor receptor, Kininogen-1, Apolipoprotein M, Angiopoietin-related protein 3, Proprotein convertase subtilisin/kexin type 9, and Lipopolysaccharide-binding protein. These findings demonstrate that chronic psychosocial stress induces alterations in plasma proteins implicated in key biological processes and pathways related to stress response, immune function, and lipid metabolic regulation. Further investigation into these proteins may provide new avenues for identification of biomarkers or mediators of stress-induced pathology.

Olfactory stimulation with multiple odorants prevents stress-induced cognitive and psychological alterations.

Acute and chronic stress markedly affects behavior by triggering sympathetic nervous system activation and several hypothalamus-pituitary-adrenal-dependent responses. Brain regions of the limbic system are responsible for the regulation of stress response, and different reports have demonstrated that their activity can be influenced by olfactory stimuli. Here we report that, in mice exposed to acute restraint stress, olfactory stimulation employing a combination of three odorants, i.e. vanillin, limonene and green odor (trans-2-hexenal and cis-3-hexenol) decreased anxiety behavior, assessed in the elevated plus maze, and halted recognition and spatial memory deficits, as appraised in two different object recognition tasks. Of note, when applied singularly, the same odorants were unable to block the detrimental effects of stress. We also found that the multiple odorants stimulation prevented the development of depressive symptoms assessed by the sucrose splash test and forced swim test in an experimental model of depression, i.e. mice exposed to a chronic unpredictable stress paradigm, and reduced interleukin 1β levels in the prefrontal cortex of depressed mice. Collectively, our data indicate that olfactory stimulation counteracts the detrimental effects of acute and chronic stress on mood regulation and cognitive functions, thus representing a potential tool for the treatment of stress-induced disorders.

Investigating the effect of chronic stress, depressive-like pathology and cognitive impairments on acute myocardial infarction: sex-differentiated effects

Abstract Background/Introduction Depression is an independent risk factor for cardiovascular disease (CVD) with the prevalence rates being higher in women than men in the general population and among patients with CVD. Furthermore, an association between myocardial infarction and cognitive deficits has been proposed, but the pathophysiological mechanisms that are responsible for the brain-heart axis interaction have not been elucidated. Purpose The present study aims to: 1) evaluate sex differences in the effect of chronic unpredictable stress (CUS) on myocardial infarct size (IS) and 2) determine the molecular pathways affected by CUS in the heart. Methods Adult male and female C57BL/6J mice, were randomly divided into 4 groups (n=7/group): CON (Control, sham surgery), iCON (Control, myocardial ischemia/reperfusion (IR)), STR (Stress, sham surgery) and iSTR (Stress, IR). Mice were intermittently exposed to the CUS protocol consisted of 4 different stressors for 6 consecutive weeks. Locomotor activity (open field-OF), anxiety-like alterations (OF, elevated plus-maze-EPM test), depressive-like pathology (tail suspension test- TST) and cognition (Y-maze and Novel Object Recognition-NOR tests) were evaluated. After behavioral evaluation, the animals were subjected to 30 min I followed by 24 h of R or sham surgery and infarct size (IS) was determined via double Evan’s Blue and triphenyltetrazolium chloride staining. In a second series of experiments (n=5/group), the ischemic part of the myocardium was collected at 24h R and subjected to label free proteomic analysis, in order to identify alterations associated with the effect of CUS and IR. Results CUS induced anxiety, depressive-like pathology and cognitive deficits as indicated by the increased time spent in the closed arms of the EPM (p<0.005), the increased immobility time (TST, p<0.05), the reduced preference for the novel object (NOR, p<0.05), and the significant body weight reduction (p<0.001), in both male and female mice. CUS significantly increased IS (p<0.001) in both male and female mice. Proteomic analysis revealed that CUS affected the heart proteome, related to endoplasmic reticulum stress, mitochondrial damage and apoptosis, of both sexes in the absence of IR. Female mice were more susceptible to IR damage in absence of CUS with 248 significant genes (FDR<0.05) being deregulated mainly belonging to Keap-Nrf2-ARE signaling pathway, in contrast to 168 significant genes in male mice. In male mice, CUS exacerbated the IR injury proteome changes mainly related to induction of apoptosis and mitochondrial dysregulation (292 significant genes, FDR<0.05 for males vs 102 for females). Conclusions Chronic exposure to stress increases depressive-like pathology and cognitive deficits, leading to heart proteome alterations and increased IS in both sexes. Sex differences were observed indicating that the coexistence of CUS and IR render the male heart more susceptible to myocardial damage.

Accumbal serotonin hypofunction and dopamine hyperfunction due to chronic stress and palatable food intake in rats

ABSTRACT Feeding is regulated by energy homeostatic and pleasure-induced rewarding signals. Palatable food intake modifies serotonergic (5-HT) and dopaminergic (DA) pathways in nucleus accumbens, inducing neuronal maladaptations that favor hyperphagia for high-energy dense food and consequent obesity. Chronic stress is an environmental condition that increases the preference for palatable food by modulating brain DA and 5-HT metabolism. Objective: To evaluate the association between changes in accumbal 5-HT and DA metabolism and the effects of chronic stress, palatable food intake and their interaction with satiety/hunger condition. Methods: Wistar rats were housed in pairs (non-stressed) or individually (stressed), fed with chow or chocolate milk plus chow (Ch) for 2 weeks (4 groups); then 6 animals/group were 48 h fasted or maintained ad libitum; the rest were fasted and re-fed for 2 h either with chow or Ch. Results: Rats with prolonged high-energy density food intake and re-fed with chow showed reduced 5-HT metabolism, although there was no association with animals’ feeding behavior. In contrast, after re-fed with palatable food, stressed chow-fed rats had increased 5-HT turnover, which decreased in Ch re-fed rats, supporting that palatable food might induce positive mood changes related to high extracellular 5-HT in limbic regions. Discussion: Rats with prolonged palatable food intake exhibited high accumbal DA turnover independently of stress exposure, supporting its relation with the development of high-energy dense food hyperphagia. As accumbal 5-HT and DA metabolism changed due to fasting or re-feeding, alterations could represent the interaction of energy homeostatic and hedonic feeding signaling in animals.

Chronic stress-mediated dysregulations in inflammatory, immune and oxidative circuitry impairs the therapeutic response of methotrexate in experimental autoimmune disease models.

Chronic stress is significantly implicated in the worsening of autoimmune disorders, contributing to elevated inflammation and diminished therapeutic efficacy. Here, in this study, we investigated the detrimental impact of an 8-week chronic unpredictable stress (CUS) protocol on the progression of arthritis and psoriasis using collagen-induced arthritis (CIA) and imiquimod (IMQ)-induced psoriasis rat models, respectively. Our objective was to elucidate how prolonged stress exacerbates disease severity and impairs the effectiveness of treatment drug. Following the induction of CIA and IMQ, rats were subjected to an 8-week CUS paradigm designed to simulate chronic stress conditions. Moreover, after 5 weeks of CUS, methotrexate (MTX; 2 mg/kg, administered once weekly for 3 weeks, intraperitoneally) was introduced as a therapeutic intervention. The severity of CUS-induced effects and the therapeutic impairment of MTX in arthritis and psoriasis rats were assessed through pathological examination of joint and epidermal tissues, respectively. Additionally, we measured various pro-inflammatory cytokine levels, including NF-κB (nuclear factor kappa B), IFN-γ (interferon-gamma), TNF-α (tumour necrosis factor alpha), IL (interleukin)-1β, IL-6, IL-17 and IL-23 using enzyme-linked immunosorbent assay (ELISA), analysed immune cells through complete haematological profiling and evaluated oxidative stress markers. Our findings revealed that CUS significantly aggravated the pathological features of both arthritis and psoriasis. Prolonged stress exposure led to heightened inflammatory responses, increased oxidative stress and more severe tissue damage. Moreover, the therapeutic efficacy of MTX was notably reduced in stressed rats compared to non-stressed, underscoring the detrimental effects of chronic stress on treatment outcomes. Taken together, our results emphasize the importance of considering chronic stress as a critical factor in the management of autoimmune diseases.

Effects of Ovarian Stimulation with Gonadotropins in the Conditions of Chronic Psychosocial Stress on the Quality of Murine Oocyte

Chronic psychosocial stress may negatively affect the female reproductive system. Meanwhile, the effect of ovarian stimulation with gonadotropins during stress on the quality of oocytes remains poorly studied. The purpose of this work was to investigate the effects of chronic psychosocial stress on the quality of murine cumulus-oocyte complexes during natural estrus cycle, as well as during ovarian stimulation with exogenous gonadotropins; the latter is an important part of modern assisted reproductive technologies. The results of the study demonstrate that psychosocial stress does not affect the number of ovulating oocytes, but worsens their quality, i. e. reduces the percentage of mature oocytes. In addition, stressed mice exhibited the increased accumulation of reactive oxygen species in oocytes, which is accompanied by the enhanced rate of apoptosis in cumulus cells. Hormonal stimulation of the ovaries with gonadotropins alleviates the negative changes associated with the psychosocial stress, normalizing the level of reactive oxygen species in oocytes and reducing the rate of apoptosis in cumulus cells.

The effects of chronic fatigue and chronic stress on alterations in immune cell responses to acute psychosocial stress

Fatigue is a common and debilitating symptom of a broad spectrum of diseases. Previous research has shown that individuals suffering from chronic forms of fatigue experience significantly more stress compared to healthy individuals, suggesting that stress is a potential pathophysiological factor in the onset and maintenance of chronic fatigue. Individually, chronic experiences of fatigue and stress have been associated with disruptions in adaptive immunity. However, how chronic fatigue and chronic stress together affect immune regulation is not fully understood. Here, we investigated the unique and combined contribution of chronic fatigue and chronic stress on immune cell redistribution in response to, and recovery from, acute psychosocial stress. Eighty women with high or low levels of chronic fatigue and varying levels of chronic stress were exposed to a psychosocial laboratory stressor. Blood samples were collected 10 min before and then at 10, 40, and 100 min after the end of stress. The main lymphocyte subpopulations (CD3+, CD3 + CD4+, CD3 + CD8+, CD16 + CD56+, and CD19 + cells) were enumerated via flow cytometry. Acute stress resulted in an increase in CD8 + and CD16+/CD56 + cells, a decline in CD4 + cells, and no effects on CD19 + B lymphocytes. Importantly, the magnitude of immune cell redistribution during stress reactivity (CD3+, CD4+, CD16+/CD56 + ) and recovery (CD3 + ) was contingent on fatigue and chronic stress levels of individuals. Notably, in contrast to low-fatigued individuals, who showed steeper changes in cell populations, increasing levels of chronic stress did not impact immune cell migration responses in high-fatigued individuals. Our findings demonstrate the compounded blunting effects of fatigue and chronic stress on adaptive immune functioning, highlighting a potential pathway for vulnerability and detrimental effects on long-term health.

Effects of Chronic Stress and Comfort Food in Testicular Morphology in Adult Wistar Rats.

To investigate the effect of chronic stress on testicular morphology in adult Wistar rats, as well as the impact of comfort food consumption on these parameters. 32 Wistar rats (10 weeks old) were divided into four groups: control (C), stressed (S), control + comfort food (C+CF), and stressed + comfort food (S+CF). Chronic stress was induced by the restraint method during 8 weeks in groups S and S+CF, while groups C and C+CF were maintained under normal conditions. Groups C and S received a standard rat chow diet, while groups C+CF and S+CF received both the standard chow and comfort food (Froot Loops®). After 8 weeks of experiment, all animals were euthanized and the testes were collected for histomorphometric, immunohistochemical and gene expression analysis. Comfort food was preferred over standard chow in groups C+CF and S+CF, but this preference was more preeminent in stressed animals (S+CF). The consumption of comfort food resulted in testicular weight reduction. The seminipherous epithelium was reduced in group S in comparison to controls. While comfort food also reduced the epithelium in C+CF in comparison to controls, for group S+CF the comfort food ameliorated the stress-induced damage. The cell proliferation rate and the relative expression of StAR and BLC2 genes were similar between the groups. Both chronic stress and comfort food consumption resulted in morphological alterations of the testes but the consumption of comfort foods during chronic stress partially prevented the stress-induced detrimental effects on testes.

Association between allostatic load and accelerated white matter brain aging: findings from the UK biobank.

White matter (WM) brain age, a neuroimaging-derived biomarker indicating WM microstructural changes, helps predict dementia and neurodegenerative disorder risks. The cumulative effect of chronic stress on WM brain aging remains unknown. In this study, we assessed cumulative stress using a multi-system composite allostatic load (AL) index based on inflammatory, anthropometric, respiratory, lipidemia, and glucose metabolism measures, and investigated its association with WM brain age gap (BAG), computed from diffusion tensor imaging data using a machine learning model, among 22 951 European ancestries aged 40 to 69 (51.40% women) from UK Biobank. Linear regression, Mendelian randomization, along with inverse probability weighting and doubly robust methods, were used to evaluate the impact of AL on WM BAG adjusting for age, sex, socioeconomic, and lifestyle behaviors. We found increasing one AL score unit significantly increased WM BAG by 0.29years in association analysis and by 0.33years in Mendelian analysis. The age- and sex-stratified analysis showed consistent results among participants 45-54 and 55-64years old, with no significant sex difference. This study demonstrated that higher chronic stress was significantly associated with accelerated brain aging, highlighting the importance of stress management in reducing dementia and neurodegenerative disease risks.

N-Pep-Zn Improves Cognitive Functions and Acute Stress Response Affected by Chronic Social Isolation in Aged Spontaneously Hypertensive Rats (SHRs).

Aging and chronic stress are regarded as the most important risk factors of cognitive decline. Aged spontaneously hypertensive rats (SHRs) represent a suitable model of age-related vascular brain diseases. The aim of this study was to explore the effects of chronic isolation stress in aging SHRs on their cognitive functions and response to acute stress, as well as the influence of the chronic oral intake of N-Pep-Zn, the Zn derivative of N-PEP-12. Nine-month-old SHRs were subjected to social isolation for 3 months (SHRiso group), and one group received N-pep-Zn orally (SHRisoP, 1.5 mg/100 g BW). SHRs housed in groups served as the control (SHRsoc). The behavioral study included the following tests: sucrose preference, open field, elevated plus maze, three-chamber sociability and social novelty and spatial learning and memory in a Barnes maze. Levels of corticosterone, glucose and proinflammatory cytokines in blood plasma as well as salivary amylase activity were measured. Restraint (60 min) was used to test acute stress response. Isolation negatively affected the SHRs learning and memory in the Barnes maze, while the treatment of isolated rats with N-Pep-Zn improved their long-term memory and working memory impairments, making the SHRisoP comparable to the SHRsoc group. Acute stress induced a decrease in the relative thymus weight in the SHRiso group (but not SHRsoc), whereas treatment with N-Pep-Zn prevented thymus involution. N-pep-Zn mitigated the increment in blood cortisol and glucose levels induced by acute stress. N-pep-Zn enhanced the adaptive capabilities towards chronic (isolation) and acute (immobilization) stress in aged SHRs and prevented cognitive disturbances induced by chronic isolation, probably affecting the hypothalamo-pituitary-adrenal, sympathetic, and immune systems.