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: 3 200
Page 80 of 320-
The Role and Mechanisms of Probiotic Supplementation on Depressive Symptoms: A Narrative Review.
PURPOSE OF REVIEW: The microbiota-gut-brain-axis (MGBA) plays a role in the aetiology of mental disorders. Depression, a leading cause of disability worldwide, may be improved by probiotics. The aim of this narrative review is to investigate and synthesize the current evidence linking probiotic food supplementation with depressive symptomology. RECENT FINDINGS: The gut and the brain communicate and interact via the MGBA through inflammation and the immune system, short chain fatty acid production, neuronal innervation and activation as well as endocrine and neurotransmitter modulation. Dysregulation of gut-brain pathways are caused by gut dysbiosis and implicated in the onset, persistence and exacerbation of depression related symptoms. Modulation of the gut microbiota via administration of probiotics has shown to reduce depressive symptom severity with Bifidobacterium and Lactobacillus strains being the most reported. Probiotics may produce greater benefits in mild depression rather than in chronic, treatment resistant depression. Probiotic supplementation is a promising and safe approach for the prevention of severe depressive disorders in high-risk individuals such as people with subthreshold depression. However, the mechanistic pathways of the MGBA require further investigation and additional human clinical trials are necessary to evaluate the role of probiotics on depression.
-
Chronic minocycline treatment exerts antidepressant effect, inhibits neuroinflammation, and modulates gut microbiota in mice.
RATIONAL: Minocycline is a second-generation, semi-synthetic tetracycline, and has broad spectrum-antibacterial activity. Interestingly, many studies have demonstrated that minocycline is beneficial for depression, which may be due to its effects on neuroinflammation modulation. Recently, gut microbiota imbalance has been found in depression patient and animal models. OBJECTIVES: Based on the fact of minocycline usually acting as an antibiotic and the relationship between depression, gut microbiota, and neuroinflammation, we designed this study to detect the effects of chronic minocycline treatment on antidepression, neuroinflammation, and gut microbiota modulation. RESULTS: Our results showed that minocycline treatment for 4 weeks, not acute treatment, exerted antidepressant effect in mice exposed to unpredictable chronic mild stress (CUMS). Further results suggested that chronic minocycline treatment inhibited neuroinflammation of hippocampus and altered species abundance and metabolites of gut microbiota. Meantime, we found that chronic minocycline treatment ameliorated intestinal barrier disruption and reduced the bacteriological indexes, such as diamine oxidase, C-reaction protein, and endotoxin in peripheral blood of CUMS mice. CONCLUSIONS: To sum up, our findings confirm that chronic minocycline treatment exerts the antidepressant effect, inhibits neuroinflammation, and modulates gut microbiota. All of these imply that the antidepressant mechanism of chronic minocycline treatment is maybe due to the combined action of neuroinflammation and gut microbiota modulation, which need further prospective studies.
-
Arbutin ameliorated depression by inhibiting neuroinflammation and modulating intestinal flora.
BACKGROUND: Arbutin (AR), a natural glycoside compound widely distributed in botanical sources, exerts neuroprotective properties. Nevertheless, the pharmacological effect of AR on depression and its underlying mechanism remain undefined. METHODS: The mice were induced by chronic unpredictable mild stress (CUMS) procedure 16S rRNA sequencing and metabolomic analyses were conducted. The in vitro neuroinflammatory model was established using lipopolysaccharide (LPS) stimulated BV2 microglia. RESULTS: The present study found that AR alleviated the depressive-like behaviors, inflammatory reaction, oxidative stress, restored neurotrophic factors and gut tight junction proteins. TLR4/NF-κB/IRAK1 signaling was involved in these alterations. 16S rRNA sequencing and metabolomics showed that AR enriched muribaculaceae and tryptophan metabolism. Muribaculum intestinale and AR ameliorated depressive-like behaviors, inflammation and 5-HT content, Tryptophan Hydroxylase 1 (TPH1) and Indoleamine 2,3-Dioxygenase 1 (IDO1) expressions, tryptophan metabolism and kynurenine route. The molecular docking and molecular dynamic suggested that AR might bind to TPH1 and IDO1. CONCLUSION: In conclusion, AR alleviated depressive-like behavior in mice by reducing neuroinflammation, modulating gut microbiota, and TPH1/IDO1-mediated serotonin synthesis.
-
Host-gut microbial metabolic crosstalk in postpartum depression: A multiomics insight linking blood metabolites to epigenetic modulation.
BACKGROUND: Recent studies suggest a link among the gut microbiota, its metabolites, and postpartum depression (PPD); however, the specific effects on host metabolism remain unclear. METHODS: A two-sample Mendelian randomization (MR) analysis was conducted using Genome-wide association study (GWAS) summary statistics on the gut microbiota and PPD. Two-step MR identified potential blood metabolites. Metabolic genes were retrieved from GeneCards. Summary data-based MR (SMR) methods integrate PPD GWAS data with blood expression quantitative trait loci (eQTLs) and DNA methylation quantitative trait loci (mQTLs) to identify key blood metabolic genes and regulatory regions linked to PPD risk. Colocalization analysis investigated interactions between host metabolic gene expression and the gut microbiota using fecal microbial quantitative trait loci (mbQTLs). RESULTS: A two-sample MR analysis revealed that class Clostridia (OR = 1.174 95% CI = 1.002-1.376 P = 0.047), order Bifidobacteriales (OR = 1.365, 95% CI: 1.073-1.735, P = 0.029), family Bifidobacteriaceae (OR = 1.365, 95% CI: 1.077-1.729, P = 0.027), genus Eggerthella (OR = 1.126 95% CI = 1.024-1.238 P = 0.014), genus Prevotella7 (OR = 1.111, 95% CI: 1.012-1.22, P = 0.026), and genus RuminococcaceaeUCG011 (OR = 1.094 95% CI = 1.009-1.185 P = 0.029) were positively correlated with PPD risk, whereas phylum Verrucomicrobia (OR = 0.881; 95% CI: 0.783-0.991; P = 0.036) had protective effects. HDL was identified as a key intermediary between Bifidobacteriales and PPD. Integrating eQTL and mQTL data, SMR revealed seven blood tissue genes (RAF1, KHK, SLC3A1, FAM3B, ALDH7A1, FDXR, and GATM) as potential causal genes for PPD and implicated specific DNA methylation sites in their regulation. Colocalization analysis revealed that FDXR, RAF1, GATM, and SLC3A1 are involved in gene-microbiota interactions. CONCLUSION: This multiomics study revealed that host metabolic genes linked to PPD are regulated through DNA methylation and metabolite-mediated host-microbiota interactions. These findings establish a foundation for future functional studies to develop mechanism-based therapeutic and preventive strategies targeting the gut-brain-metabolite axis in PPD.
-
3β-Hydroxysteroid dehydrogenase expressed by gut microbes degrades testosterone and is linked to depression in males.
Testosterone deficiency can lead to depressive symptoms in humans; however, the causes of this deficiency are incompletely understood. Here, we isolated Mycobacterium neoaurum from the fecal samples of testosterone-deficient patients with depression and showed that this strain could degrade testosterone in vitro. Furthermore, gavaging rats with M. neoaurum reduced their serum and brain testosterone levels and induced depression-like behaviors. We identified the gene encoding 3β-hydroxysteroid dehydrogenase (3β-HSD) as the enzyme causing testosterone degradation. Introducing 3β-HSD into Escherichia coli enhanced its ability to degrade testosterone. Gavaging rats with 3β-HSD-producing E. coli reduced their serum and brain testosterone levels and caused depression-like behaviors. Finally, compared with 16.67% of participants without depression, 42.99% (46/107) of the fecal samples of patients with depression harbored 3β-HSD, and 60.87% (28/46) of these fecal samples expressed 3β-HSD. These results suggest that 3β-HSD expressed by gut microbes may be associated with depressive symptoms due to testosterone degradation.
-
Neuroprotective effects of probiotics on anxiety- and depression-like disorders in stressed mice by modulating tryptophan metabolism and the gut microbiota.
Anxiety- and depression-like behaviors are commonly observed clinical features of depression and many other mental disorders. Recent evidence has revealed the crucial role of the microbiota-gut-brain axis in the bidirectional communication between the gastrointestinal tract and the central nervous system. Supplementation with psychobiotics may provide a novel approach for the adjunctive treatment of mental disorders by regulating the intestinal microecology. We isolated and identified a novel probiotic, Lactiplantibacillus plantarum D-9 (D-9), from traditional Chinese fermented foods in our previous work, which exhibited a high yield of gamma-aminobutyric acid (GABA). Herein, it was proved that the oral administration of D-9 could alleviate the depression- and anxiety-like behaviors of Chronic Unpredicted Mild Stress (CUMS) mice, and show non-toxicity or side-effects in the mice. Physiological and biochemical analyses demonstrated that D-9 regulated tryptophan metabolism, the HPA-axis and inflammation in CUMS mice. Moreover, D-9 modulated the structure and composition of the gut microbiota, leading to an increase in the relative abundance of Ligilactobacillus murinus and Lactobacillus johnsonii, and a decrease in the levels of Kineothrix alysoides and Helicobacter bilis compared to those in CUMS mice. Our work demonstrates that D-9 alleviated anxiety- and depression-like disorders in CUMS mice by modulating tryptophan metabolism and the gut microbiota. These findings provide an innovative strategy for the intervention and treatment of depressive disorders.
-
Targeting the Organ-Brain Axis: The Modulatory Role of Peripheral Organs in Depression.
Major Depressive Disorder (MDD) is a highly prevalent mental illness whose pathophysiology remains incompletely understood. Although MDD has traditionally been conceptualized primarily as a disorder of central nervous system dysfunction, accumulating evidence supports a broader brain-body framework, particularly in biologically defined subgroups characterized by inflammatory, metabolic, endocrine, autonomic, or microbiome-related abnormalities. This review summarizes how selected peripheral organs, including the gut, liver, heart, spleen, skeletal muscle, adipose tissue, bone marrow, and endocrine glands, may communicate with the brain through neural, metabolic, immune, endocrine, and microbial pathways. Emerging preclinical and clinical evidence suggests that these peripheral signals may participate in neuroinflammation and physiological alterations associated with depressive phenotypes. However, their causal status in humans remains incompletely established, and peripheral alterations may represent contributors to, correlates of, or consequences of central pathological states. We further discuss how multi-organ communication networks may converge on shared central pathways and provide a conceptual framework for understanding selected MDD phenotypes. Finally, we evaluate therapeutic strategies targeting systemic inflammation, metabolic homeostasis, and endocrine regulation, while emphasizing current translational limitations.
-
Crocetin ameliorates chronic restraint stress-induced depression-like behaviors in mice by regulating MEK/ERK pathways and gut microbiota.
ETHNOPHARMACOLOGICAL RELEVANCE: This study aimed at determining the effects of saffron on depression as well as its neuroprotective and pharmacological effects on the intestinal function of crocetin in mice exposed to chronic restraint stress. MATERIALS AND METHODS: Chronic stress was induced in two-week-old ICR mice by immobilizing them for 6 h per day for 28 days. The mice were orally administered with crocetin (20, 40, 80 mg/kg), fluoxetine (20 mg/kg) or distilled water. The treatments were administered daily and open field and tail suspension tests were performed. Immunofluorescent and Western-bolt (WB) assays were conducted to determine the expression of mitogen-activated protein kinase phosphatase-1 (MKP-1), the precursor of brain-derived neurotrophic factor (proBDNF), extracellular signal-regulated kinase 1/2 (ERK1/2), phosphorylated cAMP response element-binding (CREB) protein in the hippocampus. Serum levels of dopamine (DA), proBDNF, MKP-1 and CREB were measured by Elisa kits. High-throughput sequencing was carried out to analyze the composition of intestinal microbiota. RESULTS: Crocetin ameliorated depressive-like behaviors caused by chronic restraint stress-induced depressive mice. It significantly attenuated the elevated levels of MKP-1, proBDNF, alanine transaminase, aspartate transaminase and increased the serum levels of DA as well as CREB. Histopathological analysis showed that crocetin suppressed hippocampus injury in restraint stress mice by protecting neuronal cells. Immunofluorescent and WB analysis showed elevated expression levels of ERK1/2, CREB and inhibited expression levels of MKP-1, proBDNF in the hippocampus. The intestinal ecosystem of the crocetin group partially recovered and was close to the control group. CONCLUSIONS: Crocetin has neuroprotective properties and ameliorates the effects of stress-associated brain damage by regulating the MKP-1-ERK1/2-CREB signaling and intestinal ecosystem.
-
Effect of probiotic administration on gut microbiota and depressive behaviors in mice.
BACKGROUND: The gut microbiota is closely associated with the bidirectional gut-brain axis that modulates neuropsychological functions of the central nervous system, thereby affecting mental disorders such as depression. Although it is known that probiotics affect brain functions, the impact of probiotics on the regulation of the prevalence and composition of gut microbiota, leading to anti-depressive effects has not been well understood. METHODS: Mice were randomly divided into four different groups (n = 10 for each group) as follows: Group G1 (normal group) as control and group G2 (stress group) were given sterile saline via oral route daily for 8 weeks without and with stress condition, respectively. Under the stress condition, group G3 (fluoxetine group) was administered with fluoxetine hydrochloride and group G4 (probiotic group) was orally given multi-strains of probiotics daily for 8 weeks. After treatment, all mice underwent behavioral testing. Furthermore, fecal samples were collected from randomly selected 5 mice of each group on day 60 and taxonomical analysis of intestinal microbial distribution was performed. RESULTS: Mice subjected to restraint stress showed depressive-like behaviors along with high corticosterone levels in serum. However, probiotic administration alleviated depressive-like behaviors and decreased corticosterone level. Moreover, fecal microbiota was distinctly altered in probiotic-treated mice of the stress group. The relative abundance of phylum and genus levels was significantly decreased in the stress group, but probiotic administration restored the composition of microbes restored. CONCLUSION: Ingested probiotics alter the composition of gut microbiota, likely improving the symptoms of depression. Graphical abstract Probiotic administration alters gut microbiota and reduces depressive-like behaviors.
-
Beneficial effects of arketamine on the reduced bone mineral density in susceptible mice after chronic social defeat stress: Role of the gut-microbiota-bone-brain axis.
Patients with depression exhibit reduced bone mineral density (BMD). We previously reported that the new antidepressant arketamine improved the reduced BMD seen in chronic social defeat stress (CSDS) susceptible mice and ovariectomized mice. Considering the role of the gut microbiota in maintaining bone health, the current study investigated whether the gut microbiota, along with metabolites derived from the microbiome, play a role in the beneficial actions of arketamine with respect to the anhedonia-like behavior and reduced BMD seen in CSDS susceptible mice. A single administration of arketamine (10 mg/kg) ameliorated anhedonia-like behavior and decreased femoral neck cortical (and total) BMD in CSDS susceptible mice. There was a negative correlation between anhedonia-like behavior and BMD. Furthermore, significant differences in the abundance of microbiota (and plasma metabolites) were found between the CSDS + saline and CSDS + arketamine groups. Correlations were observed between the abundance of certain microbiota (and plasma metabolites) and cortical (and total) BMD. These data suggest that, in addition to its anti-anhedonia effect, arketamine might ameliorate the reduced cortical (and total) BMD seen in CSDS susceptible mice through the gut-microbiota-bone-brain axis. Therefore, arketamine could serve as a drug therapy for depressed patients with low BMD. This article is part of the Special Issue on "Ketamine and its Metabolites".