Acute Stress Model Research Articles

STRESS-PROTECTIVE EFFECT OF AQUEOUS INFUSION OF FERMENTED LEAVES CHAMAENERION AN-GUSTIFOLIUM (L.) SCOP.

The stress-protective effect of an aqueous infusion of fermented leaves of flowering plants of Сhamaenerion angustifolium (L.) Scop., (Onagraceae) collected in the middle taiga zone of the European North-East of Russia (near Syktyvkar), in experiments on white laboratory mice under acute stress has been studied. As a model of acute stress, the hanging of animals by the neck fold for 19 hours was used. Water infusion (1 : 20) was administered to each animal 0.5 and 1.0 ml for five days per os. It was found that the prophylactic administration of water infusion of fermented leaves in doses of 0.5 and 1.0 ml lead to normalizing effect on the mass of internal organs and peripheral blood parameters that have sharp pathological deviations under stress. The content of ascorbic acid and cholesterol in the adrenal glands and malonic dialdehyde in the liver of animals receiving infusion, approached the corresponding values in intact animals, which indicates the protective and antioxidant effects. With the introduction of sodium nitroprusside (25 mg/kg) and ethanol (25% solution, 9g/kg) a pronounced antihypoxic and antitoxic effects were found, which are typical for such well-known adaptogenic plants as ginseng and eleutherococcus. Due to data obtained, the raw material of fermented leaves of Сhamaenerion angustifolium could be considered as adaptogenic remedy that increases the overall non-specific resistance of the body and recommended not only as a tonic tea drink, but also for wider use in functional nutrition and medicine for the prevention and treatment of stress-induced and age-dependent diseases.

The effect of oligopeptides-homologs of the ACTH15-18 fragment on the adaptive response of rat blood on the acute cold stress model

Topicality. One of the important stress-protective mechanisms of oligopeptides – homologs of the ACTH15-18 fragment (under the codes KK-1 and KK-5) found in the previous studies is prevention of the hypothalamic-pituitary-adrenal system dysfunction on the acute cold stress model.Aim. To study the effect of oligopeptides – homologs of the ACTH15-18 fragment on the adaptive response of rat blood on the acute cold stress model.Materials and methods. The hemoglobin content, erythrocyte sedimentation rate, white blood cell count and leukocyte indices were studied in the blood of rats after acute cold stress.Results and discussion. Against the background of the use of peptides compared to the indicators of the control pathology group the hemoglobin content (KK-1 – by 13 % and KK-5 – by 11 %) significantly increased, while the erythrocyte sedimentation rate decreased (KK-1 – by 1.9 times and KK-5 – by 1.7 times). The peptides significantly reduced the manifestations of neutrophilia, lymphopenia and eosinopenia compared to the control pathology. Conclusions. The analysis of the experimental data indicates a significant positive effect of oligopeptides – homologs of the ACTH15-18 fragment on the adaptive response of rat blood. Preventing deep hypothermia the peptides contributed to the elimination of pathological abnormalities in the blood system. This conclusion is supported by their restorative effect on the hemoglobin level, erythrocyte sedimentation rate, white blood cell count and leukocyte indices.

A 20-hydroxyecdysone-enriched fraction from Pfaffia glomerata (Spreng.) pedersen roots alleviates stress, anxiety, and depression in mice

Ethnopharmacological relevancePfaffia glomerata roots are widely used in Brazil to treat various pathological conditions, particularly psychological disorders. 20-hydroxyecdysone, a phytosteroid present in the plant, can promote greater body resistance against exogenous and endogenous stressors. The objective of this study was to evaluate the possible neuroprotective effect of a 20-hydroxyecdysone-enriched fraction (20E-EF), obtained from P. glomerata roots, in an acute murine stress model. Material and methodsThe 20E-EF was obtained by partitioning the methanol extract from P. glomerata roots with dichloromethane. Mice were treated by gavage with three doses of 20E-EF (3, 10, and 30 mg/kg) and parameters of stress, anxiety, and depression were evaluated. Biomarkers of oxidative stress (enzymes, antioxidant profile, and oxidized molecules) were evaluated in the cortex, striatum (basal ganglia), and hippocampus of animals treated with 30 mg/kg of 20E-EF. ResultsMass spectrometry revealed that 20E was the main compound in the dichloromethane fraction. At a dose of 30 mg/kg, 20E-EF reduced stress, anxiety, and depression, while stimulating antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase), promoting antioxidant activity (antioxidant capacity, sulfhydryl groups, and reduced glutathione), and reducing oxidative markers (lipid peroxidation). In addition, 20E increased the concentration of NO in the striatum, possibly improving memory function and antioxidant activity. ConclusionA 30 mg/kg dose of 20E-EF was able to reduce stress, anxiety, and depression, in addition to maintaining antioxidant defenses of the cortex and striatum. These findings open new perspectives for understanding the therapeutic properties of P. glomerata and the underlying mechanism(s).

Protective effects of Colomast®, A New Formulation of Adelmidrol and Sodium Hyaluronate, in A Mouse Model of Acute Restraint Stress.

Stress is generally defined as a homeostatic disruption from actual or implied threats and alters the homeostatic balance of different body organs, such as gastrointestinal function and the hypothalamic-pituitary-adrenal axis (HPA), inducing the release of glucocorticoid hormones. Stress is also known to be a risk factor for the development of depression and anxiety. However, until today there are no suitable therapies for treating of stress. The aim of this study was to explore the protective effect of Colomast®, a new preparation containing Adelmidrol, an enhancer of physiological of palmitoylethanolamide (PEA), and sodium hyaluronate in an animal model of immobilization stress. Acute restraint stress (ARS) was induced in mice by fixation for 2 h of the four extremities with an adhesive tape and Colomast® (20 mg/kg) was administered by oral gavage 30 min before the immobilization. Colomast® pre-treatment was able to decrease histopathological changes in the gastrointestinal tract, cytokines expression, neutrophil infiltration, mast cell activation, oxidative stress, as well as modulate nuclear factor NF-kB and apoptosis pathways after ARS induction. Moreover, Colomast® was able to restore tight junction in both ileum and hippocampus and cortex. Additionally, we demonstrated that Colomast® ameliorated depression and anxiety-related behaviours, and modulate inflammatory and apoptosis pathways also in brain after ARS induction. In conclusion, our results suggest Colomast® to be a potential approach to ARS.

Single exercise stress reduces central neurotrophins levels and adenosine A1 and A2 receptors expression, but does not revert opioid-induced hyperalgesia in rats.

This study assessed the effects of an acute stress model upon the long-term hyperalgesia induced by repeated morphine administration in neonatal rats. We also evaluated neurotrophins and cytokines levels; expressions of adenosine and acetylcholine receptors, and acetylcholinesterase enzyme at the spinal cord. Male Wistar rats were subjected to morphine or saline administration from P8 to P14. Thermal hyperalgesia and mechanical hyperesthesia were assessed using the hot plate (HP) and von Frey (vF) tests, respectively, at postnatal day P30 and P60. After baseline measurements, rats were subjected to a single exercise session, as an acute stress model, at P30 or P60. We measured the levels of BDNF and NGF, interleukin-6, and IL-10 in the cerebral cortex and the brainstem; and the expression levels of adenosine and muscarinic receptors, as well as acetylcholinesterase (AChE) enzyme at the spinal cord. A stress exercise session was not able to revert the morphine-induced hyperalgesia. The morphine and exercise association in rats induced a decrease in the neurotrophins brainstem levels, and A1 , A2A , A2B receptors expression in the spinal cord, and an increase in the IL-6 cortical levels. The exercise reduced M2 receptors expression in the spinal cord of naive rats, while morphine prevented this effect. Single session of exercise does not revert hyperalgesia induced by morphine in rats; however, morphine plus exercise modulate neurotrophins, IL-6 central levels, and expression of adenosine receptors.

Heat stress induced oxidative damage and perturbation in BDNF/ERK1/2/CREB axis in hippocampus impairs spatial memory

Heat exposure is an environmental stress that causes diverse heat related pathophysiological changes under extreme conditions. The brain including hippocampal region which is associated with learning and memory is significantly affected by heat stress resulting in memory impairment. However, the effect of heat on the spatial memory remains unclear. The present study aimed to explore the effect of heat stress on hippocampus and spatial memory in rats. Rat model of acute heat stress was used which was divided into two groups, viz. moderate heat stress (MHS) and severe heat stress (SHS). Redox parameters evaluation revealed that MHS and SHS exposure markedly increase the production of malondialdehyde (MDA), oxidised glutathione (GSSG), reactive oxidative species (ROS), protein oxidation level and decrease the reduced glutathione (GSH) levels in the hippocampal tissue. Furthermore, Cresyl Violet (CV) staining of hippocampal region showed higher pyknosis in rats exposed to SHS. Pronounced increase of caspase3 expression and Fluoro Jade-C (FJ-C) positive cells were observed in SHS resulting in neuronal injury and apoptosis in CA3 region of hippocampus culminating in spatial memory deficit. Our data also suggest that heat stress induces phospho Extracellular signal-regulated kinases (pERK)1/2 activation induced by Brain-derived neurotrophic factor (BDNF) leading to further activation of phospho cAMP-response element binding protein (pCREB) under MHS. However, during SHS, BDNF and pCREB expression were completely dysregulated and not sufficient to rescue cognitive decline in rats. In conclusion, SHS induces pathological alterations that include oxidative damage and apoptosis of hippocampal neurons, disturbing BDNF/ERK1/2/CREB axis that may affect spatial memory.

GSB-106 Dipeptide Mimetic of Brain-Derived Neurotrophic Factor Prevents Anhedonia Development under Acute Social Defeat Stress Conditions in Mice

The influence of the dimeric dipeptide mimetic of brain-derived neurotrophic factor (BDNF) bis(N-monosuccinyl-L-seryl-L-lysine) hexamethylenediamide (GSB-106, dosage form) during three-day peroral administration at a dose of 0.1 mg/kg on the 1% sucrose solution preference test and the content of postsynaptic density protein (PSD-95) in the prefrontal cortex and hippocampus of C57Bl/6 mice was studied in an acute three-day social defeat stress model. The preference for sucrose solution decreased and the PSD-95 content in the prefrontal cortex was halved statistically significantly in stressed mice as compared to control animals. The hippocampal PSD-95 content in stressed animals did not change. Anhedonia was completely prevented after each stress session according to the sucrose preference test with peroral administration of GSB-106 at a dose of 0.1 mg/kg once per day for three days. GSB-106 did not reduce the prefrontal PSD-95 content of stressed animals during the experiment.

Circulating Steroid Changes In Response To Extreme Physical Stress In Male Athletes

PURPOSE: Athletes put themselves on a regular physical load to stay competitive. Steroids play a significant role in the regulation of cardiovascular, metabolic and many other functions in stress situations. Our aim was to monitor the response of steroid hormones to physical stress. METHODS: We investigated the plasma levels of 14 different endogenous steroid molecules in a model of extreme acute physical stress (vita maxima treadmill test) in male athletes (n=45; median age=21). Steroid levels were measured using liquid chromatography-tandem mass spectrometry. Cardiovascular-, metabolic-, and gas-exchange parameters were also evaluated. All values were measured at baseline, at maximum stress and 30 minutes into the rest period. RESULTS: The plasma concentrations of 9 steroids elevated significantly (p<0.05) at the peak compared to baseline, and 11 metabolites elevated significantly (p<0.05) in the rest period compared to baseline. After load 9 steroid showed an increase of at least 50% compared to baseline. Aldosterone showed the highest increase at peak, with 75.83%, and in the rest phase corticosterone elevated with 123.36%. Blood pressure, heart rate and lactate parameters increased significantly at the peak of the load (p<0.01). Cardiac and metabolic values did not correlate with the steroid concentrations. We calculated 11 enzyme activities from the product and substrate ratios, and we found significant differences. There were 4 enzymatic pathway which showed significant increase. 11β-HSD (p<0.01) and aldosterone-synthase (p<0.01) elevated at the peak. In the restitution 17,20-lyase and 11β-HSD in another pathway increased significantly (p<0.01). CONCLUSIONS: All three lines of the adrenal cortex are affected by extreme physical stress. Cardiovascular, metabolic and gas-exchange parameters increase early, followed by changes in the levels of endogenous steroids. as a later response. We showed for the first time in this model the elevation of some steroids, like aldosterone, corticosterone and others, and identified the enzymatic pathways involved. Literature results were partially reproduced, with further changes in steroid levels revealed by our model. This research was supported by: GINOP-2.3.2-15-2016-00047, Széchenyi 2020., 20765/3/2018 FEKUTSRAT projects.

Дипептидный миметик мозгового нейротрофического фактора ГСБ-106 предотвращает развитие ангедонии в условиях острого социального стрессаНИИ В УСЛОВИЯХ ОСТРОГО СОЦИАЛЬНОГО СТРЕССА

При моделировании острого социального стресса изучено влияние димерного дипептидного миметика мозгового нейротрофического фактора гексаметилендиамида бис(N-моносукцинил-L-серил-L-лизина) (ГСБ-106, лекарственная форма) при пероральном 3-дневном введении в дозе 0,1 мг/кг на предпочтение 1 % раствора сахара и уровень белка постсинаптической плотности PSD-95 в префронтальной коре и гиппокампе мышей С57Bl/6. У стрессированных мышей статистически значимо снижалось потребление сладкого раствора и вдвое уменьшалось содержание PSD-95 в префронтальной коре по сравнению с контрольными животными. В гиппокампе изменений содержания PSD-95 у стрессированных животных не выявлено. Введение ГСБ-106 в дозе 0,1 мг/кг перорально в течение 3 дней однократно после каждой сессии стресса полностью предотвращало развитие ангедонии по показателям потребления раствора сахара. Влияния ГСБ-106 на сниженное содержание PSD-95 в префронтальной коре стрессированных животных в период эксперимента не выявлено.

Rubiscolins: Biologically active peptides of plant origin

Two food-derived opioid peptides with high δ-opioid receptor affinity and selectivity, rubiscolin-5 and rubiscolin-6, were isolated from spinach leaves in 2001. Ribulose 1,5-bisphosphate carboxylase/oxygenase [EC 4.1.1.39 (RuBisCO)], digested by pepsin, is known as a precursor for them. The most important advantage of rubiscolins is their oral bioavailability. Both peptides produced analgesia not only after intracerebroventricular administration, but also orally. Moreover, rubiscolin-6 enhanced memory consolidation, influenced the processes of learning and memory, and reduced anxiety. In an animal model of acute stress, rubiscolin-6 induced an antidepressive-like effect. Moreover, this peptide regulated food intake, stimulated appetite in mice fed a balanced diet and suppressed food intake in case of high-fat diet. This review summarizes various biological activities of rubiscolins and recent developments on the structure-activity relationship of rubiscolin analogs, aimed at improving their pharmacological properties. Naturally occurring opioids, such as rubiscolins, can serve as the basis of new therapeutics or functional foods.

Salivary D-dimer in pigs: Validation of an automated assay and changes after acute stress

D-dimer is a peptide found in serum and is derived from the degradation of blood clots. Even though it has been analysed in human saliva, D-dimer has not been previously evaluated in the saliva of any veterinary species, and its source and role remain unknown. The objectives of this research were firstly, to validate the use of an automated method for the measurement of D-dimer in porcine saliva, and secondly, to evaluate whether D-dimer concentration changes in pig saliva after an acute stress stimulus. For this purpose, a complete analytical validation of a commercially-available immunoturbidimetric assay was carried out. In addition, an experimental acute stress model was induced in 11 pigs based on a technique involving restraint by nose-snare immobilisation for 1 min. Saliva samples were subsequently collected at different times and D-dimer, salivary alpha-amylase (sAA) and cortisol were assessed in order to evaluate changes in its concentrations after the stress induction.The D-dimer automated assay showed adequate reproducibility and sensitivity, with coefficients of variation below 10% and a limit of quantification of 0.167 μg/mL fibrinogen equivalent units (FEU). It also showed a high accuracy, determined by linearity under dilution and recovery tests. In the stress model, a significant increase (P < 0.05) in salivary D-dimer 15 min after the stress stimulus and a positive correlation between D-dimer and sAA (r = 0.51; P < 0.001) were observed. These results indicate that D-dimer can be measured in porcine saliva with an automated method and suggest that its concentration can be influenced by stressful conditions.

Restraint stress increased the permeability of the nasal epithelium in BALB/c mice

Stress seems to affect the onset and evolution of diverse illnesses with an inflammatory substrate. Whether physiological or psychological, stress increases epithelial permeability. In the mucosa of the nasal cavity and upper respiratory tract, the epithelial barrier is regulated in large part by bicellular and tricellular tight junctions (bTJs and tTJs, respectively). The junctional complexes are composed of multiple membrane proteins: claudins, tight-junction-associated MARVEL proteins (TAMs: occludin, tricellulin and marvelD3), and scaffolding proteins such as ZO-1, -2 and -3. The aim of the present study was to examine the possible modification of nasal permeability and TJ protein expression in a mouse model of acute psychological stress (a 4-h immobility session). Serum corticosterone was quantified from plasma samples to verify the onset of stress. Evaluation was made of the relative concentration of key proteins in nasal mucosa by using Western blot, and of changes in permeability by analyzing FITC-Dextran leakage from the nose to the blood. Compared to the control, the stressed group showed a greater epithelial permeability to FITC-Dextran, a reduced expression of occludin and tricellulin, and an elevated expression of ZO-2 and claudin-4. This evidence points to increased paracellular flow of large molecules through an altered structure of tTJs. Apparently, the structure of bTJs remained unchanged. The current findings could provide insights into the relation of stress to the onset/exacerbation of respiratory infections and/or allergies.

Acute Pressor Responses in Mice Exposed to Early Life Stress

Exposure to adverse childhood experiences, also known as early life stress, is an independent risk factor for the development of cardiovascular disease in adulthood. Previous studies have indicated ELS in rodents may induce impaired blood pressure regulation in response to various pro‐hypertensive stimuli. In the current study, we used maternal separation and early weaning (MSEW), a mouse model of early life stress, to determine the effects of acute behavioral stress on blood pressure regulation (n = 9/group). We utilized exposure to cage switch stress (CSS), a model of acute behavioral stress that subjects mice to a cage previously inhabited by other male mice. MSEW involves maternal separation 4h/day from postnatal days (PD) 2–5 and 8h/day from PD 6–16 then weaned at PD 17. Normally reared litters weaned at PD 21 were used as controls (CON). In normally reared CON and MSEW C57/BL6 male mice, telemetry transmitters were surgically placed with catheters in the carotid artery at 9 weeks of age. After recovery from surgery for 7–10 days, baseline measurements were recorded for 72 hours. Continuous 24 hour systolic and diastolic blood pressures (SBP and DBP) were similar between CON and MSEW mice (SBP: 125 ± 1 vs 121 ± 5 mmHg, p = 0.64; DBP: 89 ± 1 vs 91 ± 1 mmHg, p = 0.24). Additionally, exposure to MSEW did not significantly affect baseline day and night heart rate. We then subjected to CSS for 4 hours. In response to CSS, the peak change in SBP was significantly greater in MSEW mice compared to CON (39 ± 2 vs 27 ± 4 mmHg, respectively, p = 0.02). However, the total pressor response determined by area under the curve for SBP and DBP during the 30 minutes following onset of CSS and 30 minutes following the end of the 4 hour CSS exposure were similar between MSEW and CON mice. Heart rate significantly increased in both MSEW and CON mice compared to baseline (MSEW: 777 ± 10 vs 562 ± 20 bpm, p &lt; 0.0001; CON: 776 ± 4 vs 575 ± 25 bpm, p &lt; 0.0001) and thus the peak change in heart rate was not significantly different between groups (215 ± 18 vs 201 ± 23 bpm, p = 0.64). However, area under the curve analysis indicated MSEW exhibited a blunted heart rate recovery 30 minutes following the end of the 4 hours of exposure to CSS compared to CON (17998 ± 159 vs 18751 ± 287, respectively, p = 0.05). Given the changes in SBP and heart rate following CSS, these data indicate that MSEW mice have an exaggerated pressor response during exposure to acute stress. In conclusion, ELS may predispose exaggerated cardiovascular responses to stress later in life.Support or Funding InformationFunded by NIH grants HL136267 and HL69999 to D.M.P. and J.S.P. and AHA grant 17SFRN33670697 to J.S.P.

The role of hsp70 and nitrogen oxide in realization of adaptogenic reactions on the model of acute emotional stress

The role of hsp70 and nitrogen oxide in realization of adaptogenic reactions on the model of acute emotional stress

İki Kronik İmmobilizasyon Stres Protokolünün Erkek Sıçanlarda Depresyon/Anksiyete Benzeri Davranışlar Üzerine Etkilerinin Değerlendirilmesi

Objective: The effect of acute and chronic stress models on depression and/or anxiety-like behavior in rodents has been widely studied, but with contradictory results. This may be due to differences in the sex and age of the animals studied or inherent differences in the stress models used. Therefore, this study aimed to evaluate the effects of two immobilization stress protocols on depression/anxiety-like behaviors in adult male rats. Materials and Methods: Adult Wistar rats were randomly divided into three groups n=10 comprising: control, immobilization stress-1 45 minutes daily for a period of ten days , and immobilization stress-2 45 minutes twice a day for a period of ten days . Stress-related behavior was evaluated by means of the open field and forced swim tests. In addition, change in body weight, fasting blood glucose, and serum corticosterone were measured.Results: In the open field test, the percentage of time spent in the central area and mean velocity were significantly lower in the immobilization stress-1 and immobilization stress-2 groups as compared to the control group p < 0.05 and p < 0.01, respectively . Movement ratios were lower in both immobilization stress groups than in the control group p < 0.001 and p < 0.01, respectively . In the forced swim test, the duration of swimming, climbing and immobility behavior in both immobilization stress protocols did not differ from the control group. Serum corticosterone levels were higher in the immobilization stress-1 and immobilization stress-2 groups than in the control group p 0.05 . Conclusion: We may conclude that immobilization stress-1 and immobilization stress-2 protocols do not cause depression-like behavior in adult male rats. However, anxiety-like behaviors predominated in both stress protocol groups

The Molecular Signatures of Acute-immobilization-induced Antinociception and Chronic-immobilization-induced Antinociceptive Tolerance.

In the present study, the productions of antinociception induced by acute and chronic immobilization stress were compared in several animal pain models. In the acute immobilization stress model (up to 1 hr immobilization), the antinociception was produced in writhing, tail-flick, and formalin-induced pain models. In chronic immobilization stress experiment, the mouse was enforced into immobilization for 1 hr/day for 3, 7, or 14 days, then analgesic tests were performed. The antinociceptive effect was gradually reduced after 3, 7 and 14 days of immobilization stress. To delineate the molecular mechanism involved in the antinociceptive tolerance development in the chronic stress model, the expressions of some signal molecules in dorsal root ganglia (DRG), spinal cord, hippocampus, and the hypothalamus were observed in acute and chronic immobilization models. The COX-2 in DRG, p-JNK, p-AMPKα1, and p-mTOR in the spinal cord, p-P38 in the hippocampus, and p-AMPKα1 in the hypothalamus were elevated in acute immobilization stress, but were reduced gradually after 3, 7 and 14 days of immobilization stress. Our results suggest that the chronic immobilization stress causes development of tolerance to the antinociception induced by acute immobilization stress. In addition, the COX-2 in DRG, p-JNK, p-AMPKα1, and p-mTOR in the spinal cord, p-P38 in the hippocampus, and p-AMPKα1 in the hypothalamus may play important roles in the regulation of antinociception induced by acute immobilization stress and the tolerance development induced by chronic immobilization stress.

Maternal dietary supplementation with different sources of selenium on antioxidant status and mortality of chicken embryo in a model of diquat-induced acute oxidative stress

The experiment was conducted to investigate the effects of maternal dietary supplementation with different sources of selenium (Se) on antioxidant status and mortality of chicken embryo in a model of diquat-induced acute oxidative stress. A total of 180 Meihuang-4 broiler breeders (40wk old) were randomly assigned into three dietary treatments: basal diet (Control), basal diet supplemented with 0.15 mg Se/kg of sodium selenite (SS) or selenomethionine (SM)). Birds were raised for 12 wk. From 10th to 11th week of the experiments, 960 eggs were collected (40 effs per replicate) and assigned into 2 diquat-injected treatments (0 or 25 μg diquat injected on 17th day). There were 3 dietary Se treatments × 2 diquat-injected treatments (CON, SS, SM, CON-DIQ, SS-DIQ, SM-DIQ) in this experiment, each of which was replicated eight times. Then, 240 eggs were slaughtered for analysis on 18th day of hatching, and 720 eggs were used for mortality statistics on 21st day. Results showed that diquat significantly affected chicken embryos mortality and nitric oxide (NO) content, total antioxidation capability (T-AOC), protein carbonyl content, myeloperoxidase (MPO) activity, xanthine oxidase (XOD) activity, total nitric oxide synthase (NOS) activity, monoamine oxidase (MAO) activity and B-cell Leukemia Lynmphoma 2 (bcl-2) content in liver (P < 0.05). Compared with the control, broiler breeders fed with Se had lower reactive oxygen species (ROS) content, NO content, malondialdehyde (MDA) content, protein carbonyl,caspase-3 content and higher T-AOC, glutathione peroxidase (GPx) activity, mitochondrial membrane potential (MMP), MPO activity, XOD activity, MAO activity, bcl-2 content in liver (P < 0.05). There were interactions between dietary Se and diquat in chicken embryo mortality and NO content, CAT activity, MPO activity, MAO activity, caspase-3 content and bcl-2 content (P < 0.05). After diquat-injected, SM-DIQ group had lower chicken embryo mortality, NO content, caspase-3 content, bcl-2 content and higher MPO activity, MAO activity than CON-DIQ group (P < 0.05). Inconclusion, this study indicated that diquat significantly increased free radicals and induced oxidative stress in chicken embryos; maternal dietary supplementation with Se could alleviate the negative effects of diquat in chicken embryos, and SM had better protective effects against oxidative stress induced by diquat than SS.

Profiling of key brain nuclei involved in CNS control of stress and glucose homeostasis

Previous work have shown several key brain nuclei involved in acute psychological stress and glucose homeostasis. Acute stress influences glucose metabolism via released stress hormones by activating the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Little is known about the brain nuclei which response to peripheral glucose alteration are either abundant with glucosesensing neurons or the activations are secondary to stress. Here we profile and compare the brain nuclei that response to stress and glucose homeostasis in mouse models of acute restraint stress, glucose and 2-DG injections respectively. Our present work provide a comprehensive depiction on key brain nuclei involved in CNS control of stress and glucose homeostasis, which gives clue for functional identification of brain nuclei that regulate glucose homeostasis under stress.

Reduction of acute mild stress corticosterone response and changes in stress-responsive gene expression in male Balb/c mice after repeated administration of a Rhodiola rosea L. root extract.

Rhodiola rosea L. (R. rosea) is an adaptogenic plant increasing body resistance to stress. Its efficacy has been evidenced mainly in chronic stress models, data concerning its effect in acute stress and underlying mechanisms being scarce. The objective was to investigate the effect of repeated doses of a R. rosea hydroethanolic root extract (HRE) on hypothalamic pituitary adrenal response in a murine model of acute mild stress and also the mechanisms involved. Stress response was measured in Balb/c mice having received by gavage HRE (5 g/kg) or vehicle daily for 2 weeks before being submitted to an acute mild stress protocol (open‐field test then elevated plus maze). Corticosterone was measured in plasma from mandibular vein blood drawn before and 30, 60, and 90 min after initiation of the stress protocol. Mice were sacrificed at 90 min, and the hippocampus, prefrontal cortex, and amygdala were excised for high‐frequency RT‐PCR gene expression analysis. At 30 min after acute mild stress induction, corticosterone level in mice having received the HRE was lower than in control mice and comparable to that in nonstressed mice in the HRE group. HRE administration induced brain structure‐dependent changes in expression of several stress‐responsive genes implicated in neuronal structure, HPA axis activation, and circadian rhythm. In the acute mild stress model used, R. rosea HRE decreased corticosterone level and increased expression of stress‐responsive genes, especially in the hippocampus and prefrontal cortex. These findings suggest that R. rosea HRE could be of value for modulating reactivity to acute mild stress.

Modulation of the metabolic response using dexamethasone in beef steers vaccinated with a multivalent respiratory vaccine.

Available energy plays a critical role in the initiation and maintenance of an immune response to a pathogen, a process that is further altered by activation of the stress system. This study was designed to determine the effect of an acute vs chronic stress model on the metabolic response to vaccination in naïve beef steers. Steers (n = 32; 209 ± 8 kg) were blocked by body weight (BW) and randomly assigned to one of three treatments: 1) Chronic stress (CHR), 0.5 mg/kg BW dexamethasone (DEX) administered i.v. at 1000 h on day 3 to day 0; 2) Acute stress (ACU), 0.5 mg/kg BW DEX administered i.v. at 1000 h on day 0 only; or 3) Control (CON), no DEX. On day -4, steers were fitted with jugular vein catheters and moved into individual bleeding stalls in an environmentally-controlled facility. Blood samples were collected at -74, -50, and -26 h, at 0.5-h intervals from -4 to 6 h, and at 12, 24, 36, 48, and 72 h relative to vaccination with a combination vaccine (Pyramid 5 + Presponse SQ, Boehringer Ingelheim Animal Health USA, Duluth, GA) at 1200 h on day 0. Data were analyzed by the MIXED procedure of SAS specific for repeated measures. There was a treatment × time interaction (P < 0.001) for serum glucose concentrations. Specifically, glucose concentrations increased at -50 h in CHR steers and at 1200 h in ACU steers and remained elevated through 72 h postvaccination period in these two treatments compared to CON steers. The change in nonesterified fatty acid (NEFA) concentrations relative to baseline values was affected by treatment and time (P < 0.001) such that the change in NEFA was greater in CHR (0.06 ± 0.01 mmol/L), followed by CON (-0.01 ± 0.01 mmol/L) and ACU steers (-0.04 ± 0.01 mmol/L). There was a tendency (P = 0.08) for a treatment × time interaction for change in serum NEFA concentrations. Serum urea nitrogen (SUN) was affected by treatment and time (P < 0.001) such that SUN concentrations were greatest in CHR (12.0 ± 0.1 mg/dL) followed by ACU (10.4 ± 0.1 mg/dL) and CON steers (9.6 ± 0.1 mg/dL); however, the treatment × time interaction was not significant (P = 0.12). These data demonstrate that activation of the stress and immune axes using an acute or chronic stress model can increase energy mobilization prior to and following vaccination in naïve steers, potentially affecting available energy needed to mount an adequate antibody response to vaccination.