Anti-fatigue activity of fermented grain-containing blueberry anthocyanins / 军事医学

Objective To investigate the anti-fatigue activity of fermented grain-containing blueberry anthocyanins ( LANHE,LH) in mice.Methods Experiments were conducted in two phases .In the first phase , forty mice were randomly divided into four groups:control group(distilled water,dw) and three LH administration groups (8.75,17.5 and 35.08 ml/kg body mass).In the second phase, mice were randomly divided into two groups:high-dose LH group (35.08 ml/kg body mass) and control group (dw 35.08 ml/kg body mass).After four weeks, a forced swimming test was performed and the biochemical parameters related to fatigue were examined .Results and Conclusion The administration groups showed a significant increase of swimming time to exhaustion compared with the control group , especially the high-dose group ( P0.05).LH could significantly increase the liver glycogen contents and decrease the serum contents (P<0.05).These data indicate that LH has anti-fatigue activity and can elevate the exercise tolerance in mice .

Hyperhomocysteinemia is a result, rather than a cause, of depression under chronic stress.

BACKGROUND: Although the accumulation of homocysteine (Hcy) has been implicated in the pathogenesis of depression, whether Hcy is directly involved and acts as the primary cause of depressive symptoms remains unclear. The present study was designed to clarify whether increased Hcy plays an important role in stress-induced depression. RESULTS: We employed the chronic unpredictable mild stress model (CUMS) of depression for 8 weeks to observe changes in the plasma Hcy level in the development of depression. The results showed that Wistar rats exposed to a series of mild, unpredictable stressors for 4 weeks displayed depression-like symptoms such as anhedonia (decreased sucrose preferences) and a decreased 5-Hydroxy Tryptophan (5-HT) concentration in the hippocampus. At the end of 8 weeks, the plasma Hcy level increased in the CUMS rats. The anti-depressant sertraline could decrease the plasma Hcy level and improve the depression-like symptoms in the CUMS rats. RhBHMT, an Hcy metabolic enzyme, could decrease the plasma Hcy level significantly, although it could not improve the depressive symptoms in the CUMS rats. CONCLUSIONS: The results obtained from the experiments did not support the hypothesis that the increased Hcy concentration mediated the provocation of depression in CUMS rats, and the findings suggested that the increased Hcy concentration in the plasma might be the result of stress-induced depression.

Effects of HIP in protection of HSP70 for stress-induced cardiomyocytes injury and its glucorticoid receptor pathway.

Moderate levels of stress can be beneficial to health, while stress overload can cause injury or contribute to diseases. Despite a number of studies of adaptation or stress damage, the mechanisms of adaptation and stress damage remain far from clear. The effect and mechanisms of adaptation on cardiomyocytes damage caused by stress overload are discussed in this study. Data showed that mild repeated stress mitigated stress overload-induced cardiomyocyte injury both in an animal model of restraint stress and in H9C2 cells with GC (glucocorticoid) treatment. HSP70, HIP expression and interaction between HSP70 and HIP increased during adaptation induced by mild stress both in animals and H9C2 cells. Overexpression or inhibition of HSP70 in H9C2 cells with pCDNA-3.1-Hsp70 or KNK437 (HSP70 inhibitor) showed that HSP70 can protect H9C2 cells from GC-induced cell damage. A luciferase assay showed that Hsp70 plays its protective role through inhibition of GR transcription activity dependent on the interaction with HIP. These results indicated that HSP70 may promote adaptation with its interacting protein HIP, and increased levels of HSP70 and its interacting protein HIP during adaptation may play a protective role on stress-overload-induced cardiomyocyte injury.

A neuroendocrine mechanism of co-morbidity of depression-like behavior and myocardial injury in rats.

Depression is generally a recurrent psychiatric disorder. Evidence shows that depression and cardiovascular diseases are common comorbid conditions, but the specific pathological mechanisms remain unclear. The purpose of this study is to determine the effects of depression induced by chronic unpredictable mild stress (CUMS) on myocardial injury and to further elucidate the biological mechanism of depression. Rats were used as a model. The CUMS procedure lasted for a total of 8 weeks. After 4 weeks of CUMS, treated rats exhibited a reduced sucrose preference and changes in scores on an open field test, body weight and content of 5-HT in the brain as compared with the values of these variables in controls. These changes indicated depression-like changes in CUMS rats and demonstrated the feasibility of the depression model. In addition, pathological changes in the myocardium and increased cardiomyocyte apoptosis demonstrated that myocardial injury had occurred after 6 weeks of CUMS and had increased significantly by the end of 8 weeks of CUMS. Plasma serotonin (5-HT), norepinephrine (NE) and epinephrine (E), all depression-related neuroendocrine factors, were measured by HPLC-ECD techniques, and the content of plasma corticosterone (GC) was evaluated by an I(125)-cortisol radioactivity immunoassay in control and CUMS rats. The results indicated that 5-HT had decreased, whereas NE, E and GC had increased in CUMS rats, and these factors might be associated with depression-induced myocardial injury. The effects of 5-HT, NE and GC on the survival rate of cultured cardiomyocytes were determined using an orthogonal design. The results showed that 5-HT was a more important factor affecting cell survival than GC or NE. The results suggested that normal blood levels of 5-HT had a cytoprotective effect. The neuroendocrine disorders characterized by decreased 5-HT combined with increased GC and NE mediated the occurrence of depression-induced myocardial injury.

Potentral of plasma level of HSP70 as a biological marker of military stress / 军事医学

Objective To study the possibility of the plasma level of heat shock protein 70(HSP70) being used as a bi-ological marker of military stress .Methods Soldiers who returned from a 6-month-navigation were chosen as subjects , the HSP70 level of plasma was measured with the ELISA assay and stress questionnaires and Self -rated Health Measurement Scale (SRHMS) were used to measure the stress level .Results The soldiers′plasma level of HSP70 was 31.40%higher than that of the control .The stress questionnaire indicatesd that the level of thinking and anxiety , negative mood and somat-ic symptoms were higher than normal .The SRHMS indicated that the level of physiological health ,mental health and social health was lower than normal .The plasma level of HSP70 was associated with the level of military stress .Conclusion The plasma level of HSP70 may be used as an important predictor of military stress .It can predict the level of military stress injury.

Effect of different military stress loads and modes on level of stress hormones in rats / 军事医学

Objective To systematially observe the different patterns and leves of military stress on modified multitle-platform method the level of stress-related hormones in rats .Methods A sleep deprivation model was established by water environment modified multiple-platform method(MMPM).A restraint stress model was established by self-made bondage cage.Chronic unpredictable mild stress ( CUMS) model was established by action control , cage damp, cage tilt, night lightening, water and food fasting , empty bottles stimulation and group feeding methods .Cortisol, catecholamines and 5-HT levels were detected to observe the different military stress loads and modes on the level of stress hormones .Results The level of serum cortisol increased significantly ( P <0.05 ) after 5 days of sleep deprivation .The level of serum catecholamines increased significantly (P<0.05) after 1 day of sleep deprivation.The cortisol concentration increased and the level of 5-HT decreased in serum after 4 weeks CUMS.The level of catecholamines increased significantly (P<0.05) after 2-8 weeks of CUMS, increased significantly (P<0.05) after 1 week of restraint stress , and returned to normal after 3-4 weeks of restraint stress .The level of serum cortisol increased significantly after 3 -4 weeks of restraint stress . Conclusion Cortisol levels gradually increased with the level of stress in different military stress modes , which can serve as an index to evaluate the level of different stress modes .

Progress in drugs for fibrosis of important organs / 中国药理学与毒理学杂志

Fibrosis is an important pathoIogicaI change in a variety of diseases and with compIicated causes. Fibrosis diseases in different organs have different causes,but the common manifestations of fibrobIast are proIiferation and coIIagen deposition that couId eventuaIIy Iead to normaI tissue damage and Ioss of function. Fibrosis in such important organs as the heart or Iung couId be Iife-threatening. There are different reguIating factors and drugs to fibrosis. Chinese medicine treatment is stiII the main method cIinicaIIy for Iiver fibrosis. Because there is no effective cure for puImonary fibrosis,treatment focuses on anti-infIammation by aIIeviating Iesion and improving kidney function. Despite the tremendous progress in fibrosis treatment,there is stiII a Iack of targeted drugs that couId cure a specific disease in a specific area. With the deveIopment of gene technoIogy,gene therapy wiII become an important treatment for this disease. This paper introduces anti-myocardiaI fibrosis drugs according to the mechanism.

Endotoxin contamination and control in surface water sources and a drinking water treatment plant in Beijing, China.

In this paper, endotoxin contamination was determined in treated water following each unit of a drinking water treatment plant (WTP) in Beijing, China and its source water (SW) from a long water diversion channel (Shijiazhuang-Beijing) originating from four reservoirs in Hebei province, China. The total-endotoxin activities in SW ranged from 21 to 41 EU/ml at five selected cross sections of the diversion channel. The total-endotoxin in raw water of the WTP ranged from 11 to 16 EU/ml due to dilution and pretreatment during water transportation from Tuancheng Lake to the WTP, and finished water of the WTP ranged from 4 to 10 EU/ml, showing a 49% decrease following the full-scale treatment process at the WTP. Compared with the 31% removal of free-endotoxin, the WTP removed up to 71% of bound-endotoxin in raw water. The traditional treatment processes (coagulation, sedimentation and filtration) in the WTP removed substantial amounts of total-endotoxin (up to 63%), while endotoxin activities increased after granular activated carbon (GAC) adsorption and chlorination. The total-endotoxin in the actual water was composed of free-endotoxin and bound-endotoxin (endotoxin aggregates, bacteria-bound endotoxins and particle-attached endotoxins). The endotoxin aggregates, bacteria-bound endotoxins and particle-attached endotoxins co-exist as suspended particles in water, and only the bacteria-bound endotoxins were correlated with bacterial cells suspended in water. The particle distribution of endotoxin aggregates in ultrapure water was also tested and the results showed that the majority (64-89%) of endotoxin aggregates had diameters <2 µm. The endotoxin contamination and control in treated water following each unit of the WTP processes and its SW from reservoirs are discussed and compared with regard to bacterial cell counts and particle characteristics, which were dependent, to a certain extent, on different flow rates and turbulence of the water environments.

Phosphorylated nerve growth factor-induced clone B (NGFI-B) translocates from the nucleus to mitochondria of stressed rat cardiomyocytes and induces apoptosis.

Stress induces cardiac dysfunction and cardiomyocyte injury, and while current data indicate that mitochondria play a key role in this process, the mechanisms remain unknown. In this study, we found that in rats, restraint stress induced nerve growth factor-induced clone B (NGFI-B) translocation from the nucleus to mitochondria in cardiomyocytes. This translocation promoted cytochrome c release from mitochondria to the cytoplasm, which ultimately resulted in cardiomyocyte apoptosis. We also found that stress induced oversecretion of glucocorticoids and activated the protein kinase A (PKA) pathway in cardiomyocytes. Enhanced PKA activity increased NGFI-B serine phosphorylation, which caused NGFI-B to translocate from the nucleus to mitochondria. Moreover, a PKA peptide inhibitor blocked NGFI-B serine phosphorylation and translocation. Our data demonstrate that stress affects cardiomyocytes by inducing NGFI-B mitochondrial translocation via serine phosphorylation, which in turn initiates mitochondrial-mediated apoptosis.

Comparative Proteomics Analysis of Hippocampal Proteins From Chronic Stressed Rats / 生物化学与生物物理进展

Chronic stress can induce hippocampus injury such as neuron loss, dendrite atrophy, but its mechanism and molecular basis remain unclear up to now. To understand the molecular mechanism on protein level and find the crucial proteins which correlated with chronic stress-induced injury, two-dimensional electrophoresis was applied to separate the hippocampal total proteins of control group and restraint stressed rats, then the differential expressed proteins were detected by image analysis and identified by matrix assisted laser desorption /ionization time of flight mass spectrometry (MALDI-TOF-MS) as well as database searching. Moreover, the 2-DE results were verified on the mRNA level by semi-quantitative RT-PCR. The hippocampal 2-DE map with high resolution and good reproducibility of control and stress group rats were obtained. Fourteen differentially expressed protein spots were detected and eleven proteins were successfully identified, most of these proteins were involved in the process of energy metabolism and signal transduction. These results provide a clue for elucidating the mechanism of chronic stress-induced hippocampal injury and are useful for elevating the adaptability to stress.

Protective effect of heat-stress preconditioning on anoxic endothelial cells and its mechanism / 中国病理生理杂志

AIM: To observe the protective effect of heat stress preconditioning on endothelial cells under anoxia and explore its mechanism. METHODS: The endothelial cells were divided into 4 groups: (1) anoxia; (2) heat stress; (3) heat stress preconditioning + hypoxia; (4) control. LDH activity was measrued by using Automatic Biochemistry Analysis-Meter. Cell death rate was determined by trypan blue, NO production was tested by measuring NO - 2/NO - 3 content in cellular culture medium by using Griess assay. RESULTS: LDH release and cell death rate of the anoxia endothelial cells significantly increased compared with control; 39℃ heat stress preconditioning reduced those increment by 29、47%, 33.67% respectively. 41℃ heat stress preconditioning has no protection against the anoxia-induced injury in endothelial cells. The NO production in anoxic endothelial cells decreased markedly. 39℃ heat stress preconditioning induced the increase in NO production in endothelial cells, but 41℃ heat stress preconditioning made the NOS activity decrease. The NO production was correlated negatively with LDH release and cell death rate in anoxic endothelial cells. CONCLUSION: The heat stress preconditioning within the limits can protect the endothelial cells from anoxia injury. The increase in NO in endothelial cells may play an important role in the mechanism of the protective effect.

Mitochondrial membrane mechanism of rat heart injury induced by stress / 中国病理生理杂志

AIM: To investigate the effects of stress on the opening of mitochondrial membrane permeability pore (PTP) in rat heart and explore the possible molecular mechanism underlying PTP opening. METHODS: Stress animal model was established. After strained for differnet time, all rats were killed and PTP opening degree were examined by spectrophotometer. Bcl-2, Bax expression levels were determined by Western blot. RESULTS: Stress induced PTP opning, Bcl-2 expression inhibition and Bax level elevation in myocardial mitochondria. CONCLUSION: PTP opening was the important mitochondrial mechanism of stress-induced heart injury. Decrease in Bcl-2 expression and increase of Bax level may be an important molecular basis for PTP opening.