Браузер не даёт сохранять данные (например, приватный режим): закладки пропадут после закрытия вкладки.
Поиск статей PubMed
Ключевые слова, автор, журнал, годы — результаты из PubMed, аннотации с переводом на русский, закладки в браузере.
Найдено: 3 201
Страница 118 из 321-
An Almond-Based Low Carbohydrate Diet Improves Depression and Glycometabolism in Patients with Type 2 Diabetes through Modulating Gut Microbiota and GLP-1: A Randomized Controlled Trial.
BACKGROUND: Alow carbohydrate diet (LCD) is more beneficial for the glycometabolism in type 2 diabetes (T2DM) and may be effective in reducing depression. Almond, which is a common nut, has been shown to effectively improve hyperglycemia and depression symptoms. This study aimed to determine the effect of an almond-based LCD (a-LCD) on depression and glycometabolism, as well as gut microbiota and fasting glucagon-like peptide 1 (GLP-1) in patients with T2DM. METHODS: This was a randomized controlled trial which compared an a-LCD with a low-fat diet (LFD). Forty-five participants with T2DM at a diabetes club and the Endocrine Division of the First and Second Affiliated Hospital of Soochow University between December 2018 to December 2019 completed each dietary intervention for 3 months, including 22 in the a-LCD group and 23 in the LFD group. The indicators for depression and biochemical indicators including glycosylated hemoglobin (HbA1c), gut microbiota, and GLP-1 concentration were assessed at the baseline and third month and compared between the two groups. RESULTS: A-LCD significantly improved depression and HbA1c (p <0.01). Meanwhile, a-LCD significantly increased the short chain fatty acid (SCFAs)-producing bacteria Roseburia, Ruminococcus and Eubacterium. The GLP-1 concentration in the a-LCD group was higher than that in the LFD group (p <0.05). CONCLUSIONS: A-LCD could exert a beneficial effect on depression and glycometabolism in patients with T2DM. We speculate that the role of a-LCD in improving depression in patients with T2DM may be associated with it stimulating the growth of SCFAs-producing bacteria, increasing SCFAs production and GPR43 activation, and further maintaining GLP-1 secretion. In future studies, the SCFAs and GPR43 activation should be further examined.
-
The Impact of Weizmannia coagulans BC99 on Anxiety and Depression: An 8-Week Clinical Pilot Study Through the Gut Microbiota-Brain Axis.
Background: An imbalance in the immune system, stress response, and gut microbiota can contribute to the onset and progression of anxiety and depression. This pilot study aimed to explore the effect of Weizmannia coagulans BC99 on anxiety and depression through the gut microbiota-brain axis. Methods: A total of 79 participants with Hamilton Depression Rating Scale (HAMD-17) ≥ 8 or Hamilton Anxiety Rating Scale (HAMA-14) ≥ 7 were included and completed the study. The participants were randomly assigned to either the placebo group or the BC99 intervention group. The intervention lasted 8 weeks, with participants receiving either dextrin (3 g/day) or BC99 probiotics (3 g/day, 5 × 109 CFU) daily. Pre- and post-intervention comparisons were made on HAMD and HAMA scores, inflammatory cytokines, neurotransmitters, gut microbiota, and short-chain fatty acids. Results: Results showed that after 8 weeks, BC99 and placebo intervention were effective in reducing HAMD and HAMA scores, and HAMD and HAMA scores in BC99 group were reduced by 2.40 and 5.53 points compared the placebo group, and the response and remission rates were also higher than that of the placebo, but there was no significant difference. BC99 also could regulate the levels of inflammatory cytokines IL-17 and IL-10, and increase neurotransmitter levels of γ-GABA and NO. Moreover, compared with the placebo group, BC99 also enhanced the abundance of beneficial bacteria such as Faecalibactrium, Megamonas, Dialister, and Agathobacter, which were closely associated with clinical indicators of mental disorders, and increased the production of short-chain fatty acids. Conclusions: These preliminary findings suggested that BC99 might alleviate anxiety and depression symptoms by regulating the level of neurotransmitters or the change of microbiota, which needed further verification in subsequent animal or clinical experiments.
-
Time-Dependent Multisystem Effects of Small Independent Space (SIS) Exposure in Mice: Integrative Analysis of Behavior, Neuroendocrine, Gut Microbiota, and Hippocampal Function.
Exposure to small independent space (SIS) causes stress-related behavioral and neural abnormalities, but the time-dependent mechanisms and gut microbiota-hippocampus interactions remain unclear. To investigate the time-dependent effects of acute and chronic restraint stress (CRS) on mouse behavior, neuroendocrine function, gut microbiota, and hippocampal activity. Behavioral assessments were conducted using the open field test and tail suspension test. Meanwhile, enzyme-linked immunosorbent assay (ELISA) was applied to measure neurotransmitters, hypothalamic-pituitary-adrenal (HPA) axis markers, and inflammatory factors; 16S rRNA sequencing was used for gut microbiota analysis; liquid chromatography-tandem mass spectrometry (LC-MS/MS) for metabolite identification; and immunofluorescence staining for hippocampal structure observation. Acute SIS induced depression-like behaviors. Chronic SIS showed peak despair at 4 days (d), followed by persistent depression at 8 d. Norepinephrine (NE) increased while 5-hydroxytryptamine (5-HT) decreased; NE depletion at 4 d coincided with reduced hippocampal glucocorticoid receptor (GR) expression. Both acute (2 h) and chronic (4 d) SIS reduced gut microbiota diversity and disrupted tyrosine metabolism. Hippocampal tests showed neuronal compensation at 6 h post-acute stress and neuronal apoptosis with glial dysfunction after 4 d of chronic stress. SIS damages via the "gut microbiota-tyrosine metabolism-hippocampus axis," with 4 d of chronic exposure as a critical decompensation point, offering a time-specific intervention target.
-
Galacto-oligosaccharides ameliorate polystyrene nanoplastic-induced anxiety- and depression-like behaviors via a gut-initiated serotonergic cascade.
As emerging environmental contaminants, micro- and nanoplastics (MNPs) raise neurotoxic concerns. However, the mechanisms underlying their induction of emotional disorders remain poorly understood. In particular, intervention-oriented and functionally validated strategies for prevention and control are still lacking. To address this, we conducted a 28-day repeated oral exposure study in mice using a gradient of polystyrene nanoplastics (PS-NPs; 2, 10, and 50 mg/kg/day) spanning environmentally relevant doses, systematically assessing impacts along the microbiota-gut-brain axis. Our results showed that PS-NP exposure induced dose-dependent anxiety- and depression-like behaviors, with fluorescence tracing revealing predominant gut accumulation and limited brain distribution. Mechanistically, exposure induced gut microbiota dysbiosis, intestinal barrier impairment, and lipopolysaccharide translocation, ultimately leading to systemic inflammation and neuroinflammation. Serum biochemical analysis showed that gut dysbiosis initiates host tryptophan metabolism toward the kynurenine pathway by triggering inflammation and subsequent indoleamine 2,3-dioxygenase 1(IDO1) activation. Consistently, hippocampal transcriptomic and biochemical analyses confirmed decreased 5-HT levels and suppression of the downstream 5-HT1A-cAMP-PKA-CREB-BDNF neurotrophic cascade, demonstrating comprehensive serotonergic disruption from substrate depletion to receptor dysfunction. Notably, the prebiotic galacto-oligosaccharides (GOS) restored intestinal homeostasis and ameliorated these anxiety- and depression-like behavioral and metabolic deficits, exerting protective effects by counteracting the above pathway. Our work delivers a from-mechanism-to-solution understanding: it deciphers how microplastics disrupt the gut-brain axis to cause neurotoxicity and identifies GOS maintenance of intestinal health as a key mitigative strategy against plastic pollution risks. Therefore, maintaining intestinal health, particularly through dietary GOS, represents a viable strategy to mitigate the neurotoxicity induced by plastic pollution.
-
GV-971 Ameliorates Chronic Restraint Stress-Induced Depression-like Phenotypes Accompanied by Reshaping of the Microbiota-Gut-Brain Axis.
Depression is increasingly linked to microbiota-gut-brain axis dysfunction, yet current monoaminergic antidepressants show limited efficacy. This study investigated the therapeutic potential and underlying mechanisms of GV-971, a marine-derived oligosaccharide, in a chronic restraint stress (CRS) mouse model. We first established that 8 h of daily restraint for 4-8 weeks induces a stable depression-like phenotype characterized by behavioral despair and significant reduction in peripheral monoamine neurotransmitters (5-HT and norepinephrine). GV-971 treatment robustly attenuated CRS-induced depression- and anxiety-like behaviors, restored hippocampal serotonin levels, reduced elevated plasma corticosterone concentrations, and ameliorated CRS-induced adrenal cortical hyperplasia. Mechanistically, GV-971 significantly suppressed neuroinflammation by inhibiting microglial hyperactivation in the prefrontal cortex and hippocampus. Concurrently, it repaired intestinal barrier dysfunction, evidenced by reduced permeability, restored mucosal integrity, and recovered goblet cell numbers. Crucially, integrated shot-gun metagenomics and plasma metabolomics revealed that GV-971 not only reshaped microbial taxonomy but also functionally recalibrated the gut ecosystem. It enriched beneficial taxa (e.g., Bifidobacterium pseudolongum, Bacteroides uniformis) and specific metabolic pathways, leading to increased short-chain fatty acids (valeric and caproic acids) and a significant reduction in plasma levels of tryptophan-kynurenine pathway metabolites, specifically the neurotoxic compounds kynurenine and quinolinic acid. Fecal microbiota transplantation (FMT) from GV-971-treated donors partially recapitulated the antidepressant and gut-protective effects in CRS recipients, confirming a causal role for the remodeled microbiota. Collectively, GV-971 exerts antidepressant effects by coordinately remodeling the gut microbiota, normalizing tryptophan and SCFA metabolism, restoring gut barrier integrity, and dampening central neuroinflammation, supporting its potential as a novel gut-brain axis-targeted therapy for depression.
-
Antioxidant Carbon Dots Nanozymes Alleviate Stress-induced Depression by Modulating Gut Microbiota.
Depression is a debilitating mental illness that severely threatens millions of individuals and public health. Because of the multifactorial etiologies, there is currently no cure for depression; thus, it is urgently imperative to find alternative antidepressants and strategies. Growing evidence underscores the prominent role of oxidative stress as key pathological hallmarks of depression, making oxidative stress a potential therapeutic target. In this study, we report a N-doped carbon dot nanozyme (CDzyme) with excellent antioxidant capacity for treating depression by remodeling redox homeostasis and gut microbiota. The CDzymes prepared via microwave-assisted fast polymerization of histidine and glucose exhibit superior biocompatibility. Benefiting from the unique structure, CDzymes can provide abundant electrons, hydrogen atoms, and protons for reducing reactions, as well as catalytic sites to mimic redox enzymes. These mechanisms collaborating endow CDzymes with broad-spectrum antioxidant capacity to scavenge reactive oxygen and nitrogen species (•OH, O2-•, H2O2, ONOO-), and oxygen/nitrogen centered free radicals. A depression animal model was established by chronic unpredictable mild stress (CUMS) to evaluate the therapeutic efficacy of CDzymes from the behavioral, physiological, and biochemical index and intestinal flora assessments. CDzymes can remarkably improve depression-like behaviors and key neurotransmitters produced in hippocampus tissues and restore the gut microbiota compositions and the amino acid metabolic functions, proving the potential in treating depression through the intestinal-brain axis system. This study will facilitate the development of intestinal flora dysbiosis nanomedicines and treatment strategies for depression and other oxidative stress related multifactorial diseases.
-
Multi-omics approach identifies gut microbiota variations associated with depression.
The gut microbiota plays a potential role in the pathophysiology of depression through the gut-brain axis. This cross-sectional study in 400 participants from the PREDIMED-Plus study investigates the interplay between gut microbiota and depression using a multi-omics approach. Depression was defined as antidepressant use or high Beck Depression Inventory-II scores. Gut microbiota was characterized by 16S rRNA sequencing, and faecal metabolites were analysed via liquid chromatography-tandem mass spectrometry. Participants with depression exhibited significant differences in gut microbial composition and metabolic profiles. Differentially abundant taxa included Acidaminococcus, Christensenellaceae R-7 group, and Megasphaera, among others. Metabolomic analysis revealed 15 significantly altered metabolites, primarily lipids, organic acids, and benzenoids, some of which correlated with gut microbial features. This study highlights the interplay between the gut microbiota and depression, paving the way for future research to determine whether gut microbiota influences depression pathophysiology or reflects changes associated with depression.
-
The Microbiome in Mental Health: Potential Contribution of Gut Microbiota in Disease and Pharmacotherapy Management.
The gut microbiome is composed of ~10(13) -10(14) microbial cells and viruses that exist in a symbiotic bidirectional communicative relationship with the host. Bacterial functions in the gut have an important role in healthy host metabolic function, and dysbiosis can contribute to the pathology of many medical conditions. Alterations in the relationship between gut microbiota and host have gained some attention in mental health because new evidence supports the association of gut bacteria to cognitive and emotional processes. Of interest, illnesses such as major depressive disorder are disproportionately prevalent in patients with gastrointestinal illnesses such as inflammatory bowel disease, which pathologically has been strongly linked to microbiome function. Not only is the microbiome associated with the disease itself, but it may also influence the effectiveness or adverse effects associated with pharmacologic agents used to treat these disorders. This field of study may also provide new insights on how dietary agents may help manage mental illness both directly as well as though their influence on the therapeutic and adverse effects of psychotropic agents.
-
Inflammatory cytokines and prenatal depression: Is there a mediating role of maternal gut microbiota?
OBJECTIVE: The mechanism of levels of inflammatory cytokines that affects brain function and mood through gut microbiota has not been fully elucidated. This study aimed to investigate the potential mediating role of gut microbiota between maternal inflammatory cytokines levels and prenatal depression. DESIGN: There were 29 women in the prenatal depression group and 27 women in the control group enrolled in this study. The Edinburgh Postnatal Depression Scale (EPDS) score of 10 was considered the cut-off value for prenatal depression. We collected demographic information, stool and blood samples. The gut microbiota was profiled using V3-V4 gene sequence of 16S rRNA, and the concentration of inflammatory cytokines were analyzed. The mediation model was analyzed by using the model 4 in the process procedure for SPSS. RESULTS: There were significance differences in the concentration of interleukin-1beta (IL-1β)(Z = -2.383, P = 0.017) and IL-17A (Z = -2.439, P = 0.015) between the prenatal depression group and control group. There was no significant difference in α- diversity and β-diversity between the two groups. Intestinibacter (OR: 0.012; 95% CI, 0.001-0.195) and Escherichia_Shigella (OR: 0.103; 95% CI, 0.014-0.763) were protective factors for prenatal depression, while Tyzzerella (OR: 17.941; 95% CI, 1.764-182.445) and Unclassified_f_Ruminococcaceae (OR: 22.607; 95% CI, 1.242-411.389) were risk factors. And Intestinibacter play a mediation effect between IL-17A and prenatal depression. CONCLUSION: Maternal gut microbiota is a significant mediator of the relationship between inflammatory cytokines and prenatal depression. Further research is still needed in exploring the mediating mechanisms of gut microbiota between inflammatory cytokines and depression.
-
Effects of spleen nerve denervation on depression-like phenotype, systemic inflammation, and abnormal composition of gut microbiota in mice after administration of lipopolysaccharide: A role of brain-spleen axis.
BACKGROUND: Accumulating evidence suggests the role of brain-spleen axis as well as brain-gut-microbiota axis in inflammation-related depression. The spleen mediates anti-inflammatory effects of the vagus nerve which plays a role in depression. However, the role of spleen nerve in inflammation-related depression remains unclear. METHODS: The effects of the splenic nerve denervation (SND) in the depression-like phenotype, systemic inflammation, and abnormal composition of gut microbiota in adult mice after administration of lipopolysaccharide (LPS) were examined. RESULTS: LPS (0.5 mg/kg) caused depression-like phenotype, systemic inflammation, splenomegaly, increased expression of Iba1 (ionized calcium-binding adapter molecule 1) and decreased expression of postsynaptic density protein-95 (PSD-95) in the hippocampus in the sham-operated mice. In contrast, LPS did not produce depression-like phenotype, and abnormal expressions of Iba1 and PSD-95 in the hippocampus in the SND-operated mice. Furthermore, SND significantly blocked LPS-induced increased plasma levels of pro-inflammatory cytokine interleukin-6 although SND did not affect LPS-induced splenomegaly and increased plasma levels of tumor necrosis factor-α in mice. There were significant changes in several microbiota among the four groups. Interestingly, there were correlations between the relative abundance of several microbiota and Iba1 (or PSD-95) expression in the hippocampus. In addition, expression of Iba1 in the hippocampus was correlated with the relative abundance of several microbiota. LIMITATIONS: Detailed mechanisms are unclear. CONCLUSIONS: These results suggest that the splenic nerve plays a role in inflammation-related depression, microglial activation in the hippocampus, and that gut microbiota may regulate microglial function in the brain via gut-microbiota-brain axis.