Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An increased systemic concentration of stress hormones (of the hypothalamic-pituitary adrenal axis) and some cytokines may contribute to the depression of immune cell function typically observed after prolonged exercise. The aim of the present study was to determine the effect of 2 weeks of supplementation with vitamin C (VC) on cortisol, adrenocorticotrophic hormone, interleukin-6, oxidative stress and neutrophil responses to a single bout of endurance exercise. Nine healthy endurance-trained males exercised for 2.5 h at 60% VO2max after 2 weeks of placebo (PLA) or VC (1,000 mg day(-1)) supplementation. All participants completed both trials utilising a randomised crossover design with a minimum 14 day washout period between trials. There was a significant trial x time interaction effect for plasma cortisol concentration (P = 0.039) which tended to be lower in the VC trial but post hoc analysis found no specific between trial differences. There was a significantly lower post-exercise neutrophilia (P < 0.014) in the VC trial, compared with the PLA trial. There was no trial x time interaction for measures of neutrophil function (bacteria-stimulated elastase release, fMLP or PMA-stimulated oxidative burst). However, there was a trend for higher fMLP-stimulated neutrophil oxidative burst in the VC compared with PLA trial (trial x time interaction, P = 0.075). These results suggest that supplementation with VC for a period of up to 2 weeks provides little to no protection against the depression of neutrophil function which typically occurs after endurance exercise.
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PMID:The effect of 2 weeks vitamin C supplementation on immunoendocrine responses to 2.5 h cycling exercise in man. 1721 67

The longer life expectancy of women than that of men and, therefore, the longer exposure to fracture risk has, at least partially, led to neglect of osteoporosis in men. Recently, unipolar depression, which is 2 times more frequent in women than in men, has been linked to osteoporosis. However, it is quite possible that this diagnosis may escape detection in men because of a different behavioral phenotype between the genders. A potential mechanism of bone loss in depression has been proposed, involving concurrent activation of the hypothalamo-pituitary-adrenal and sympatho-adrenal axes, suppression of the gonadal and somatotrophic axes, and high interleukin-6 and low leptin levels. We suggest that similar neurohormonal changes may cause osteoporosis in men.
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PMID:Depression and osteoporosis in men: association or casual link? 1672 81

Cytokine-dependent mechanisms in the CNS have been implicated in the pathogenesis of depression. Interleukin-6 is upregulated in depressed patients and dowregulated by antidepressants. It is, however, unknown whether IL-6 is involved in the pathogenesis of depression. We subjected IL-6-deficient mice (IL-6(-/-)) to depression-related tests (learned helplessness, forced swimming, tail suspension, sucrose preference). We also investigated IL-6 in the hippocampus of stressed wild-type mice. IL-6(-/-) mice showed reduced despair in the forced swim, and tail suspension test, and enhanced hedonic behavior. Moreover, IL-6(-/-) mice exhibited resistance to helplessness. This resistance may be caused by the lack of IL-6, because stress increased IL-6 expression in wild-type hippocampi. This suggests that IL-6 is a component in molecular mechanisms in the pathogenesis of depression. IL-6(-/-) mice represent tools to study IL-6-dependent signaling pathways in the pathophysiology of depression in vivo. Moreover, these mice may support the screening of compounds for depression by altering cytokine-mediated signaling.
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PMID:IL-6 knockout mice exhibit resistance to stress-induced development of depression-like behaviors. 1684

Cytokines are important mediators of cardiac disease. Accumulating evidence indicates that members of the interleukin-6 family of cytokines promote cardiac hypertrophy through the activation of the Janus kinase-signal transducer and activator of transcription (Jak/STAT) pathway. Aberrant Jak/STAT signaling may promote progression from hypertrophy to heart failure. Suppressor of cytokine signaling (SOCS) proteins are underexplored, negative regulators of Jak/STAT signaling. SOCS proteins may also interact with other inflammatory pathways known to affect cardiac function. A better understanding of the therapeutic potential of these proteins may lead to the controlled progression of heart failure and the limitation of myocardial depression. This review summarizes the cardiophysiological effect of the IL-6 cytokine family, outlines the mechanistic pathway of Jak/STAT signaling, explores the regulatory role of SOCS proteins in the heart, and discusses the potential of using SOCS proteins clinically.
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PMID:Jak/STAT/SOCS signaling circuits and associated cytokine-mediated inflammation and hypertrophy in the heart. 1691 47

Patients undergoing cancer treatment (e.g., interferon or IL-2 treatment) develop depression, and there is a positive relationship between their depression and circulating levels of proinflammatory cytokines. Depressed patients who are medically healthy also show increases in circulating markers of inflammation. The present study characterized baseline levels of inflammatory cytokine activity in 18 pairs of depressed and non-depressed persons at high risk for cancer and matched for age, ethnicity and all unaffected by a personal history of cancer. Circulating levels of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), tumor necrosis factor-alpha-receptor (TNF-RII), and soluble intercellular adhesion molecule (sICAM) did not differ between those with and without depression. The present data are important for characterizing persons at high risk for cancer who may later acquire knowledge of further increased risk through genetic testing.
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PMID:Pro-inflammatory cytokines and depression in a familial cancer registry. 1709 69

Icariin is one of the major active flavonoids constituents of Epimedium brevicornum MAXIM (Berberidaceae). Icariin and E. brevicornum have a wide range of pharmacological activities. Abnormality in the hypothalamic-pituitary-adrenal (HPA) axis is considered to be a key neurobilogical factor in major depression, and cytokines have a close relationship with the activation of the HPA axis. In the present study, the aim was to determine whether icariin possesses an antidepressant-like activity, and to explore the effects of icariin on the HPA axis and cytokine levels in chronic mild stress (CMS) model of depression in Sprague-Dawley rats. Icariin significantly increased the sucrose intake of CMS-treated rats from week 3. It not only attenuated the CMS-induced increases in serum corticotropin-releasing factor (CRF) and cortisol levels, but also reversed the abnormal levels of serum interleukin-6 (IL-6) and tumor-necrosis-factor alpha (TNF-alpha) to the normal in the stressed rats. These results suggested that icariin possessed an antidepressant-like property that was at least in part mediated by neuroendocrine and immune systems.
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PMID:Effects of icariin on hypothalamic-pituitary-adrenal axis action and cytokine levels in stressed Sprague-Dawley rats. 1714 71

Previous studies have demonstrated that Xuezhikang, an extract of cholestin, available from Chinese red yeast rice, could effectively modify lipid profile. The present study was undertaken to investigate whether Xuezhikang could modify endothelin-1 (ET-1), interleukin-6 (IL-6), high-sensitivity C-reactive protein (CRP) and exercise-induced ischemia in patients with cardiac syndrome X (CSX). Thirty-six patients with CSX were randomly assigned to 1200 mg/d of Xuezhikang or placebo group (n=18 respectively). Blood samples were drawn at day 0 and day 90 for measuring above parameters. The treadmill exercise tests and subjective feelings were also assessed at day 0 and day 90. The data showed that Xuezhikang therapy resulted in significant reductions in total cholesterol (TC, 19%), low-density lipoprotein cholesterol (LDL-C) (26%), and triglycerides (TG) compared with baseline (16%, p<0.01 respectively). The data also showed that Xuezhikang led significantly to reductions in median and log-CRP levels (38% and 44%, p<0.01 respectively), IL-6 (20%, p<0.01), and ET-1 (47%, p<0.01) compared with baseline. The exercise duration, and time to 1 mm ST-segment depression was significantly prolonged after Xuezhikang therapy (9% and 6%, p<0.05 respectively) accompanied by improvement of subjective feelings. Data suggested that the benefit of Xuezhikang resulted in significant modification vascular function by reduction of ET-1, inflammatory markers and LDL cholesterol, which may be clinically important for patients with CSX.
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PMID:Xuezhikang, an extract of cholestin, decreases plasma inflammatory markers and endothelin-1, improve exercise-induced ischemia and subjective feelings in patients with cardiac syndrome X. 1719 75

Severe or chronic disease can lead to cachexia which involves weight loss and muscle wasting. Cancer cachexia contributes significantly to disease morbidity and mortality. Multiple studies have shown that the metabolic changes that occur with cancer cachexia are unique compared to that of starvation. Specifically, cancer patients seem to lose a larger proportion of skeletal muscle mass. There are three pathways that contribute to muscle protein degradation: the lysosomal system, cytosolic proteases and the ubiquitin (Ub)-proteasome pathway. The Ub-proteasome pathway seems to account for the majority of skeletal muscle degradation in cancer cachexia and is stimulated by several cytokines including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interferon-gamma and proteolysis-inducing factor. Cachexia is particularly severe in pancreatic cancer and contributes significantly to the quality of life and mortality of these patients. Several factors contribute to weight loss in these patients, including alimentary obstruction, pain, depression, side effects of therapy and a high catabolic state. Although no single agent has proven to halt cachexia in these patients there has been some progress in the areas of nutrition with supplementation and pharmacological agents such as megesterol acetate, steroids and experimental trials targeting cytokines that stimulate the Ub-proteasome pathway.
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PMID:Mechanisms of skeletal muscle degradation and its therapy in cancer cachexia. 1745 54

Circumstantial evidence has suggested that activated microglia may be associated with the pathogenesis of depression. Pro-inflammatory cytokines may also be involved. Therefore, we examined the effects of various types of antidepressants, as well as the mood-stabilizer lithium chloride, on interferon-gamma (IFN-gamma)-induced microglial production of the pro-inflammatory mediators interleukin-6 (IL-6) and nitric oxide (NO). Treatment of the murine microglial 6-3 cells with 100 U/ml of IFN-gamma resulted in an eightfold increase in IL-6 and a tenfold increase in NO into the culture medium. Pretreatment with the selective serotonin reuptake inhibitor fluvoxamine, the relatively selective noradrenaline reuptake inhibitor reboxetine, or the non-selective monoaminergic reuptake inhibitor imipramine, significantly inhibited IL-6 and NO production in a dose-dependent manner. These inhibitions were reversed significantly by SQ 22536, a cyclic adenosine monophosphate (cAMP) inhibitor, and, except for reboxetine, by the protein kinase A (PKA) inhibitor Rp-adenosine3',5'-cyclic monophosphorothioate triethylammonium salt (Rp-3',5'-cAMPS). Lithium chloride, which is believed to act by inhibiting the calcium-dependent release of noradrenaline, had a different spectrum of action on microglial 6-3 cells. It enhanced IFN-gamma-stimulated IL-6 production and inhibited NO production. The inhibitory effect of lithium chloride was not reversed by either SQ 22536 or Rp-3',5'-cAMPS. These results suggest that antidepressants have inhibitory effects on IFN-gamma-activated microglia and these effects are, at least partially, mediated by the cAMP-dependent PKA pathway. On the other hand, the mood stabilizer and anti-manic agent lithium chloride has mixed effects on IFN-gamma-induced microglial activation.
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PMID:Antidepressants inhibit interferon-gamma-induced microglial production of IL-6 and nitric oxide. 1748 8

An association or a casual link has been proposed between the neuroendocrinological and neuroimmunological changes attributed to either depression or cancer. This study investigated whether breast cancer patients with and without major depression exhibit plasma interleukin-6 abnormalities and dexamethasone suppression test results. Four groups, each consisting of 30 women (1--healthy women, 2--patients with major depression, 3--breast cancer patients without major depression, 4--breast cancer patients with major depression), were compared to each other. Psychiatric evaluations were made by structured clinical interview for DSM-IV. Severity of depression was measured with the Hamilton Depression Rating Scale. Plasma levels of interleukin-6 were measured. A dexamethasone suppression test was applied. Breast cancer patients with major depression had markedly higher plasma levels of interleukin-6 than the other group. All breast cancer patients with depression had abnormal dexamethasone suppression test results. These findings suggest a hypothalamo-pituitary-adrenal axis activation and plasma levels of interleukin-6 and plasma interleukin-6 elevation and plasma levels if interleukin-6 and plasma levels of post cortisol concentrations. Evidence for a casual link or association of major depression with immune and endocrinological activation needs to be investigated further.
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PMID:Interleukin-6 levels and HPA axis activation in breast cancer patients with major depressive disorder. 1758 77


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