Your browser does not allow saving data (e.g. private mode): bookmarks will be lost when the tab closes.
Search PubMed
Keywords, author, journal, years — results from PubMed, abstracts with Russian translation, bookmarks in your browser.
Found: 3 201
Page 116 of 321-
The relationship between sleep, gut microbiota, and metabolome in patients with depression and anxiety: A secondary analysis of the observational study.
BACKGROUND: Growing attention is paid to the association between alterations in the gut microbiota and their metabolites in patients with psychiatric disorders. Our study aimed to determine how gut microbiota and metabolomes are related to the sleep quality among patients with depression and anxiety disorders by analyzing the datasets of our previous study. METHODS: Samples were collected from 40 patients (depression: 32 patients [80.0%]); anxiety disorders: 8 patients [20.0%]) in this study. Gut microbiomes were analyzed using 16S rRNA gene sequencing and gut metabolomes were analyzed by a mass spectrometry approach. Based on the Pittsburgh Sleep Quality Index (PSQI), patients were categorized into two groups: the insomnia group (PSQI score ≥ 9, n = 20) and the non-insomnia group (PSQI score < 9, n = 20). RESULTS: The insomnia group showed a lower alpha diversity in the Chao1 and Shannon indices than the non-insomnia group after the false discovery rate (FDR) correction. The relative abundance of genus Bacteroides showed a positive correlation with PSQI scores in the non-insomnia group. The concentrations of glucosamine and N-methylglutamate were significantly higher in the insomnia group than in the non-insomnia group. CONCLUSIONS: Our findings suggest that specific taxa could affect the sleep quality among patients with depression and anxiety disorders. Further studies are needed to elucidate the impact of sleep on specific gut microbiota and metabolomes in depression and anxiety disorders.
-
Nutritional Interventions for Perimenopausal Anxiety and Depression Targeting Tryptophan and GABA Pathways: A Narrative Review.
This narrative review examines perimenopause as a critical transitional phase in women's lives, often accompanied by elevated vulnerability to anxiety and depression. Dysfunction of the gut-brain axis is one of the key factors contributing to perimenopausal mood disorders and is currently receiving extensive attention. GBA dysfunction can trigger neurotransmitter metabolic imbalance, intestinal barrier impairment, and neuroinflammatory responses. Tryptophan (Trp) and γ-aminobutyric acid (GABA) serve as essential precursors and direct modulators of key neurotransmitters, and the dysregulation of their metabolic pathways has been implicated in perimenopausal anxiety and depression in animal models and limited clinical observations. Trp influences 5-hydroxytryptamine (5-HT) by affecting emotional states. GABA is the primary inhibitory neurotransmitter in the central nervous system and is closely associated with anxiety and depression. Fluctuations in estrogen levels during perimenopause significantly alter the composition and metabolic activity of the gut microbiota, which in turn affects Trp metabolism and GABA synthesis through increased intestinal permeability, activation of immune-inflammatory responses, and disruption of hypothalamic-pituitary-adrenal (HPA) axis function. Although traditional hormone replacement therapy and pharmacological treatments are effective, they are associated with some side effects. Preliminary evidence from in vitro and animal studies suggests that nutritional interventions targeting Trp and GABA metabolism within the gut-brain axis may offer a novel research direction, though their efficacy in perimenopausal women remains to be established. Potential nutritional strategies, including supplementation with Trp and its precursors, inhibition of the kynurenine pathway (KP), and supplementation with probiotics and prebiotics, can modulate Trp and GABA metabolism. This review focuses on Trp and GABA metabolic regulation via the gut-brain axis to explore pathogenesis of perimenopausal anxiety and depression and summarize potential nutritional intervention targets, thereby providing a scientific basis for emotional management in perimenopausal women.
-
Dietary sulforaphane glucosinolate alleviates stress-induced depression and demyelination through gut-brain axis modulation.
Chronic stress is a major risk factor for depression and white matter injury, yet effective preventive strategies remain limited. Here, we investigated whether an 8-week diet supplemented with 0.1% sulforaphane glucosinolate (SGS) could prevent depression-like behaviors and corpus callosum (CC) demyelination in C57BL/6 mice exposed to 14 d of chronic restraint stress (CRS). SGS pre-treatment significantly reduced immobility in the forced swim test and showed a trend toward preserving sucrose preference compared with stressed controls. Consistently, Black-Gold II staining and myelin basic protein (MBP) immunofluorescence demonstrated that SGS markedly attenuated CRS-induced myelin loss in the corpus callosum. Gut microbiota profiling by 16S rRNA sequencing revealed unchanged α-diversity but clear β-diversity shifts, including enrichment of taxa such as Lacrimispora and Roseburia in SGS-fed mice under CRS. Untargeted plasma metabolomics further showed that SGS normalized stress-elevated metabolites, and correlation analyses linked specific microbial taxa and metabolites to myelin integrity. Together, these findings indicate that dietary SGS confers stress resilience and preserves white matter integrity, at least in part, through modulation of the gut-brain axis. SGS therefore represents a promising nutraceutical strategy for the prevention of stress-related neuropsychiatric and white matter disorders.
-
Integrative fMRI and multiomics reveal neuroprotective mechanisms of Astragalus membranaceus in sleep deprivation-induced depression.
BACKGROUND: Sleep deprivation (SD) is a significant public health concern and a risk factor for neuropsychiatric disorders, including depression. SD disrupts the gut-brain axis, causing dysbiosis and neuroinflammation. Astragalus membranaceus (AST) exhibits antidepressant and anti-inflammatory properties, including modulation of the gut microbiota; however, its neuroprotective effects on SD-induced neuropsychiatric disturbances remain largely unexplored. This study investigates the potential of AST using an innovative integrative multiomics approach. PURPOSE: This study was conducted to investigate the neuroprotective effects of AST against SD-induced depression-like behavior and to explore the mechanism underlying its regulatory effects on the gut-brain axis. METHODS: We established a chronic SD mouse model that was subjected to AST intervention and employed a pioneering integrative multiomics approach-combining resting-state functional magnetic resonance imaging for brain function, metagenomics for microbiota profiling, metabolomics for metabolic alterations, and transcriptomics for gene expression in key brain regions. Behavioral tests and cytokine assays complemented these analyses to comprehensively evaluate the therapeutic effects of AST. RESULTS: SD induced depression-like behavior, neuroinflammation (IL-1β, IL-6, and TNF-α secretion), gut dysbiosis (Proteobacteria expansion, loss of beneficial microbes), and disrupted metabolic pathways. AST alleviated behavioral deficits, normalized brain connectivity, and reduced the levels of proinflammatory cytokines. It also reshaped microbiota, enriching Muribaculum and Butyricicoccus, and restored metabolic profiles, increasing the levels of short-chain fatty acids and promoting bile acid pathways. Integrated analysis linked microbiota restoration to reduced neuroinflammation and improved neuroprotection. CONCLUSION: AST modulates the gut-brain axis to counteract SD-induced dysbiosis, neuroinflammation, and metabolic imbalance, alleviating depression-like symptoms. These findings offer novel mechanistic insights into the therapeutic potential of AST for SD-related neuropsychiatric conditions.
-
Cydonia oblonga Mill. Fruit Extract Ameliorates Lipopolysaccharide-Induced Depression-like Behaviors in Mice by Modulating Inflammation, Metabolites and Gut Microbiota.
BACKGROUND: Cydonia oblonga Mill. is rich in flavonoid compounds and shows potential for application in functional foods. This study investigated the therapeutic potential of hydroethanolic extract of Cydonia oblonga Mill. fruit (HECO) in alleviating lipopolysaccharide (LPS)-induced depression-like behaviors in mice. METHODS: Mice were treated with HECO (600 mg/kg, p.o.) for 21 consecutive days. From day 14 to day 21, depression-like behavior was induced by LPS (2.0 mg/kg injected i.p.). Behavioral parameters and biochemical markers were then assessed. Gut microbiota composition was analyzed by 16S rRNA gene sequencing, and serum metabolites were profiled through untargeted metabolomics. RESULTS: HECO improved LPS-induced behavioral alterations, including increased locomotor activity in the open-field test and decreased immobility time in the forced swimming test and tail suspension test, and reduced serum IL-6 levels in LPS-treated mice. Furthermore, HECO markedly upregulated the expression of occludin and ZO-1 in the hippocampus and inhibited neuroinflammation by suppressing activation of the TLR4/MyD88/NF-κB signaling pathway. HECO significantly increased the relative abundance of Deferribacterota in LPS-induced mice. A total of 262 differential metabolites were identified between the LPS and HECO groups, with the top potential biomarkers predominantly categorized into lipids, flavonoid-containing phenylpropanoids, organic acids, and peptides. CONCLUSIONS: HECO improved depression-like behavior in LPS-induced mice, potentially through modulation of gut microbiota and serum metabolites, attenuation of systemic inflammation, and inhibition of the TLR4/MyD88/NF-κB signaling pathway in the hippocampus.
-
Minocycline alters behavior, microglia and the gut microbiome in a trait-anxiety-dependent manner.
Major depressive disorder is the main cause of disability worldwide with imperfect treatment options. However, novel therapeutic approaches are currently discussed, from augmentation strategies to novel treatments targeting the immune system or the microbiome-gut-brain axis. Therefore, we examined the potential beneficial effects of minocycline, a tetracycline antibiotic with pleiotropic, immunomodulatory action, alone or as augmentation of escitalopram on behavior, prefrontal microglial density, and the gut microbiome in rats selectively bred for high anxiety-like behavior (HAB). We show that concomitant with their high innate anxiety and depression, HABs have lower microglial numbers in the infralimbic and prelimbic prefrontal cortex and an altered gut microbiota composition compared with controls. Three weeks of minocycline treatment alleviated the depressive-like phenotype, further reduced microglial density, exclusively in male HAB rats, and reduced plasma concentrations of pro-inflammatory cytokines. However, coadministration of escitalopram, which had no effect alone, prevented these minocycline-induced effects. Moreover, minocycline led to a robust shift in cecal microbial composition in both HABs and rats non-selected for anxiety-like behavior. Minocycline markedly increased relative abundance of Lachnospiraceae and Clostridiales Family XIII, families known for their butyrate production, with a corresponding increase and positive correlation in plasma 3-OH-butyrate levels in a trait-dependent manner. Thus, our data suggest that the antidepressant effect of minocycline is sex- and trait-dependent, associated with a reduced microglial number in the prefrontal cortex, and with changes in microbial composition and their metabolites. These results further support the microbiome-gut-brain axis as potential target in the treatment of depression.
-
Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation.
PURPOSE: Gut microbiota regulate intestinal function and health. However, mounting evidence indicates that they can also influence the immune and nervous systems and vice versa. This article reviews the bidirectional relationship between the gut microbiota and the brain, termed the microbiota-gut-brain (MGB) axis, and discusses how it contributes to the pathogenesis of certain disorders that may involve brain inflammation. METHODS: Articles were identified with a search of Medline (starting in 1980) by using the key words anxiety, attention-deficit hypersensitivity disorder (ADHD), autism, cytokines, depression, gut, hypothalamic-pituitary-adrenal (HPA) axis, inflammation, immune system, microbiota, nervous system, neurologic, neurotransmitters, neuroimmune conditions, psychiatric, and stress. FINDINGS: Various afferent or efferent pathways are involved in the MGB axis. Antibiotics, environmental and infectious agents, intestinal neurotransmitters/neuromodulators, sensory vagal fibers, cytokines, and essential metabolites all convey information to the central nervous system about the intestinal state. Conversely, the hypothalamic-pituitary-adrenal axis, the central nervous system regulatory areas of satiety, and neuropeptides released from sensory nerve fibers affect the gut microbiota composition directly or through nutrient availability. Such interactions seem to influence the pathogenesis of a number of disorders in which inflammation is implicated, such as mood disorder, autism-spectrum disorders, attention-deficit hypersensitivity disorder, multiple sclerosis, and obesity. IMPLICATIONS: Recognition of the relationship between the MGB axis and the neuroimmune systems provides a novel approach for better understanding and management of these disorders. Appropriate preventive measures early in life or corrective measures such as use of psychobiotics, fecal microbiota transplantation, and flavonoids are discussed.
-
The influence of washed microbiota transplantation on menstruation in female patients of childbearing age.
BACKGROUND AND AIMS: Menstrual disorders are closely related to the disorder of gut microbiota. This study aims to explore the impact of Washed microbiota transplantation (WMT) on the quality of life, depression and anxiety scale scores, and menstrual conditions of female patients of childbearing age. METHODS: The data of female patients of childbearing age who received WMT at the First Affiliated Hospital of Guangdong Pharmaceutical University from February 2023 to February 2025 were collected. A comparative analysis was conducted on the effects of SF-36, SDS, SAS and menstrual conditions in female patients of childbearing age before and after WMT treatment. The changes of gut microbiota before and after WMT were analyzed by 16S rRNA gene sequencing. RESULTS: A total of 23 female patients of childbearing age were included in this study. WMT significantly improved the scores of GH, SF, MH, RE and VT in SF-36 of female patients of childbearing age and significantly reduced the scores of SDS and SAS (P < 0.05). The MDQ score was negatively correlated with the PF, BP, GH, VT, RE and MH scores in SF-36, and positively correlated with the SDS and SAS scores (P < 0.05). WMT enhanced the α diversity of gut microbiota in female patients of childbearing age, and the Chao1 and Shannon indices were statistically significant (P < 0.05). At the same time, the relative abundance of Dialister, Bifidobacterium, Faecalibacterium, Roseburia and Fusobacterium increases. The relative abundances of Bacteroides, Agathobacter, Prevotella, Escherichia-Shigella and Ruminococcus decreased. CONCLUSIONS: WMT treatment can effectively improve the quality of life score of female patients of childbearing age and reduce the scores of depression and anxiety scales. WMT can increase the diversity and abundance of gut microbiota in female patients of childbearing age and improve menstrual conditions, which provides new ideas for future clinical treatment.
-
Role of 5-Hydroxytryptamine and Intestinal Flora on Depressive-Like Behavior Induced by Lead Exposure in Rats.
OBJECTIVE: To investigate the effects of 5-hydroxytryptamine (5-HT) and intestinal flora on depression-like behavior induced by lead exposure in rats. METHODS: 30 healthy SPF adult male SD rats were randomly divided into control group and lead exposure group. The depression-like behavior of rats was detected. The blood, striatum, and intestinal tissue were collected. The lead content was detected by ICP-MS. The mRNA expressions of ChgA, TPH1, 5-HT, and 5-HT3R were tested by qRT-PCR. The content of 5HT was checked by HPLC-ECD. The content of 5-HT3R was detected by ELISA. The protein expressions of 5-HT, 5-HT3R, ChgA, and TPH were gauged by immunohistochemistry. Fecal samples were collected, and the composition of intestinal flora in experimental rats was analyzed by 16 s RNA metagene sequencing. RESULTS: Lead exposure can greatly cause depression. The content of 5-HT in blood and striatum in the lead exposure group decreased, and the expression levels of 5-HT, 5-HT3 R, ChgA, and TPH in the intestine decreased distinctly. Compared with the control group, the distribution of a-polymorphism related indexes Simpson, Chao1, Shannon, and ACE in rats with depressive-like behavior after lead exposure was significantly increased; in the lead exposure group, there were 61 different operational taxonomic units (OUTs) in intestinal flora at the family level. Based on linear discriminant analysis, it was found that the key bacteria were Lactobacillaceae and Bifidobacteriaceae, and their abundance decreased evidently in the lead exposure group. CONCLUSION: Lead exposure improves depressive-like behavior by affecting intestinal flora and regulating neurotransmitter 5-HT through the intestinal-brain axis.
-
Dysregulation of the microbiota-gut-brain axis induced by chronic pancreatitis mediates anxiety- and depression-like behaviors in mice.
BACKGROUND: Anxiety and depression are common psychological complications in patients with chronic pancreatitis (CP). This study aims to investigate the dysregulation of microbiota-gut-brain axis induced by CP in driving anxiety- and depression-like behaviors in mice. METHODS: C57BL/6J mice injected with caerulein (Cae) were used to establish an experimental CP model. Behavioral tests were performed to assess anxiety- and depression-like behaviors. The gut microbiota composition and serum metabolites were analyzed via 16S rRNA sequencing and liquid chromatography-mass spectrometry, respectively. Antibiotic cocktail (ABX) and fecal microbiota transplantation (FMT) models were employed to validate the direct role of the gut microbiota, while mixed probiotic gavage was used for intervention evaluation. RESULTS: Cae-injected mice presented typical CP symptoms and significant anxiety- and depression-like behaviors. 16S rRNA sequencing revealed altered gut microbiota composition in CP mice, with a reduced abundance of Lactobacillus and enrichment of Helicobacter. ABX and FMT experiments confirmed that the CP-derived gut microbiota can independently induce anxiety/depression-like behaviors. In CP mice, Serum corticosterone and its metabolite levels were significantly increased in CP mice. CP-induced microbiota dysbiosis can induce the downregulation of intestinal barrier and blood-brain barrier functions, increase inflammatory levels, and extensively dysregulate neurotransmitter transmission in the brain. Treatment with mixed probiotics improved anxiety- and depression-like behaviors in CP mice. CONCLUSIONS: CP promotes anxiety- and depression-like behaviors in mice by inducing gut microbiota dysbiosis. This study provides experimental evidence for the use of microbiota-targeted interventions for treating the psychological complications of CP.