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Gut-derived commensal bacteria attenuate corticosterone-induced depressive-like behavior via regulation of oxidative stress and mitochondrial apoptotic signalling.
Chronic stress and sustained glucocorticoid exposure disrupt intracellular signaling networks that regulate mitochondrial function and neurotrophic support, thereby increasing vulnerability to depressive disorders. Among these alterations, redox imbalance and mitochondrial dysfunction contribute to impairment of neuronal survival pathways, including TrkB-ERK-CREB-BDNF signaling. However, upstream biological modulators of these stress-responsive processes remain incompletely understood. Here, we investigated whether gut-derived commensal bacteria function as modulators of neuronal signaling under chronic stress conditions. Using a fecal microbiota transplantation (FMT)-based behavioral stratification approach, we identified Intestinimonas butyriciproducens and Parabacteroides merdae as species depleted in mice with increased depressive-like immobility. Functional validation showed that both strains attenuated oxidative stress, reduced intracellular reactive oxygen species, and suppressed mitochondrial apoptotic signaling in neuronal cells, accompanied by restoration of TrkB-ERK-CREB signaling and increased brain-derived neurotrophic factor expression. In a chronic corticosterone model, oral administration of these strains reduced depressive-like behavior and restored hippocampal BDNF levels. Collectively, these findings demonstrate that defined commensal bacteria act as biological modulators of intracellular signaling pathways, including redox balance and mitochondrial function, thereby preserving neurotrophic signaling. This study provides evidence linking specific commensal taxa to modulation of neuronal signaling under chronic stress conditions.
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Changes in Gut Microbiota by Chronic Stress Impair the Efficacy of Fluoxetine.
Major depressive disorders (MDDs) constitute a leading cause of disability worldwide and current pharmacological treatments are partially effective. The gut microbiota (GM) has recently emerged as a target of therapeutic interest for MDDs. In this study, we transfer GM from mice that sustained unpredictable chronic mild stress (UCMS) to healthy recipient mice. The fecal transfer induces despair-like behavior, decreases neurogenesis in the hippocampus (HpC), and impairs the antidepressant and neurogenic effects of a standard selective serotonin (5-HT) reuptake inhibitor, fluoxetine (FLX). These effects are paralleled by deficits in 5-HT bioavailability, biosynthesis, and reuptake in the HpC. Treatment with 5-hydroxytryptophan restores the levels of 5-HT and its precursors in the HpC, improves HpC neurogenesis, and alleviates despair-like symptoms. Our results reveal that stress-induced changes in GM are involved in the pathogenesis of depressive disorders and minimize FLX efficacy via alterations in the serotonergic pathway of Trp metabolism.
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Bupleurum polysaccharide improves CUMS-induced depressive behavior in rats by regulating the "microbiota-gut-brain Axis": a mechanism study based on metabolomics and metagenomics.
This study aimed to comprehensively investigate the antidepressant mechanisms of Bupleurum polysaccharide (BP) through the microbiota-gut-brain axis, employing an integrated multi-omics approach. Using a chronic unpredictable mild stress (CUMS) rat model of depression, we evaluated BP's effects on depressive-like behaviors and analyzed its regulatory mechanisms on metabolites and gut microbiota through combined metabolomics and metagenomics. Structural characterization revealed that Bupleurum polysaccharide SPAP-1 is an acidic homogeneous polysaccharide with a molecular weight of approximately 100 kDa, primarily composed of glucose, mannose, rhamnose, and other monosaccharides. Pharmacodynamic assessments demonstrated that BP significantly ameliorated CUMS-induced depressive behaviors, including weight loss, reduced food intake, anhedonia, and behavioral despair (P < 0.05). Metabolomic analysis identified 19 differential metabolites, with BP reversing 11 of them, primarily involved in phenylalanine and tryptophan metabolism pathways. Western blot analysis confirmed BP's regulatory effects on key enzymes Got1 and Lta4h. Metagenomic results showed that BP remarkably reshaped gut microbiota structure, restored microbial diversity, optimized the Firmicutes/Bacteroidetes ratio, enriched beneficial genera (Agathobacter, Phocaeicola), and inhibited pathogenic genera (Ruminococcus). Crucially, integrated multi-omics analysis revealed significant microbiota-metabolite correlations, demonstrating that BP-promoted beneficial bacteria positively correlated with neurotransmitter precursors, while BP-inhibited pathogenic bacteria associated with pro-inflammatory mediators. Mediation analysis further established the "microbiota → metabolite → behavior" causal chain, with Ruminococcus → LTB4 → despair behavior accounting for 42.3 % of the mediation effect. In conclusion, Bupleurum polysaccharide ameliorates depressive-like behaviors through multi-target regulation of the metabolite-microbiota interaction network, highlighting its potential as an antidepressant agent or functional food and providing a novel research paradigm for understanding the multi-target characteristics of traditional Chinese medicine polysaccharides.
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Hydrogen Therapy and Lipopolysaccharide Trapping with MgB2@Inulin Gel for Reversing Colitis and Its Associated Psychiatric Complications via the Gut-Brain Axis.
Individuals diagnosed with inflammatory bowel disease (IBD) frequently encounter dysbiosis of the intestinal microbiota and are predisposed to psychiatric comorbidities, such as depression and anxiety. The development of oral therapeutics that concurrently attenuate intestinal inflammation, modulate gut microbiota, and ameliorate psychiatric symptoms is imperative for effective IBD management. This study introduced an orally administered Inulin gel incorporating magnesium diboride nanosheets (MgB2@Inulin gel). The hydrolysis of MgB2 nanosheets could generate reductive hydrogen gas (H2), which is critical for scavenging excess reactive oxygen/nitrogen species (RONS), and boron ions that neutralize harmful lipopolysaccharides (LPS). Prebiotic Inulin could effectively protect MgB2 nanosheets from gastric acid degradation, ensuring their persistence in the intestinal tract, where it modulated the gut microbiota and preserved intestinal barrier integrity. Notably, MgB2@Inulin gel markedly alleviated anxiety and depressive behaviors in the model of colitis by regulating the gut-brain axis. Thus, this work underscores the pivotal role of the gut-brain axis in the therapeutic approach to IBD and its associated psychiatric manifestations, proposing a straightforward, safe, and efficacious oral hydrogen treatment strategy for IBD and concurrent mental health disorders.
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Association of escitalopram-induced shifts in gut microbiota and sphingolipid metabolism with depression-like behavior in wistar-kyoto rats.
The microbiota-gut-brain axis plays a pivotal role in neuropsychiatric disorders, particularly in depression. Escitalopram (ESC) is a first-line antidepressant, however, its regulatory mechanisms on the microbiota-gut-brain axis in the treatment of depression remain unclear. The antidepressant effects of ESC were evaluated using the forced swim test in Wistar-Kyoto (WKY) rats, while damage in the gut and brain regions was assessed through H&E staining and immunohistochemistry. The therapeutic mechanisms in WKY rats with depression-like behavior were investigated through 16S rRNA sequencing of the gut microbiota, serum untargeted metabolomics, and hippocampal proteomics. Results indicated that ESC intervention improved depressive-like behaviors, as evidenced by increased swimming times in WKY rats, and also restored intestinal permeability and brain tissue integrity. Significant changes in the gut microbiota composition, particularly an increase in Bacteroides barnesiae, as well as increases in serum sphingolipid metabolites (Sphinganine 1-phosphate, Sphingosine, and Sphingosine-1-phosphate) and hippocampal proteins (Sptlc1, Enpp5, Enpp2), were strongly correlated. These robust correlations suggest that ESC may exert its antidepressant effects by modulating sphingolipid metabolism through the influence of gut microbiota. Accordingly, this research elucidates novel mechanisms underlying the antidepressant efficacy of ESC and highlights the pivotal importance of the microbiota-gut-brain axis in mediating these effects.
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Schisandra chinensis ameliorates depressive-like behaviors by regulating microbiota-gut-brain axis via its anti-inflammation activity.
The present study aimed to examine the antidepressant actions of the composition fractions of Schisandra chinensis using LPS-induced mice. Animals were treated with total extracts (SCE), lignans (SCL), polysaccharides (SCPS), and essential oil (SCVO), and then subjected to behavioral tests. The forced swimming test (FST) and tail suspension test (TST) were used as predictive animal models of antidepressant activity. Total extracts and lignans significantly decreased the duration of immobility in FST and TST. We found that treatment with SCE and SCL could significantly decrease the levels of pro-inflammatory cytokines both in the periphery and central nervous system (CNS). This was confirmed by the histopathological examination of the colon. The RT-PCR results demonstrated that SCE and SCL could greatly inhibit the TLR4/NF-κB/IKKα signaling pathway. In addition, the concentrations of Butyric acid and Propionic acid were upregulated by the administration, and the decreased diversity of intestinal microbiota and alterations of the relative proportions of Bacteroidetes and Firmicutes phylum members, Barnesiella and Lactobacillus genus members in LPS-induced mice were restored as well. All results suggested that lignans is the effective fraction of S.chinensis to ameliorating depressive disorders, which its anti-inflammation activity possibly involved in the bidirectional connection between gut microbiota and brain.
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Gut microbiota mediates the antidepressant-like effects of xiaochaihutang: mechanisms involving inhibition of inflammation and enhancement of barrier function.
Depression is a common mental disorder that seriously impairs the psychological and physical health of patients. Extensive research has indicated that patients with depression exhibit disturbances in their gut microbiota. Xiaochaihutang (XCHT) is a traditional herbal recipe widely used in China, and previous studies have found it to possess antidepressant properties. However, whether XCHT can modulate depression-associated gut microbiota dysbiosis remains unclear. In this research, we investigated the impact of XCHT on the microbiota-gut-brain axis in depressed rats and elucidated the potential mechanisms. A rat model of depression was established using the chronic unpredictable mild stress (CUMS) protocol. Behavioral tests demonstrated that XCHT significantly alleviated depression-like behaviors. 16S rRNA sequencing revealed that XCHT enhanced the diversity and compositional structure of the gut microbiota and specifically increased the abundance of the beneficial bacterium Blautia. Fecal microbiota transplantation (FMT) experiments further confirmed that the antidepressant-like effects of XCHT were mediated through modulation of the gut microbiota. Furthermore, XCHT exhibited anti-inflammatory properties in both the central and peripheral systems and improved the integrity of the intestinal barrier and the blood-brain barrier. These mechanisms were also validated using the FMT approach. Collectively, these findings suggest that the antidepressant-like mechanism of XCHT may be directly linked to the regulation of the microbiota-gut-brain axis. This study demonstrates that XCHT exerts antidepressant-like effects by modulating the microbiota-gut-brain axis, providing novel insights into the potential therapeutic mechanisms and clinical applications for depression.
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Dietary sulforaphane glucosinolate mitigates depression-like behaviors in mice with hepatic ischemia/reperfusion injury: A role of the gut-liver-brain axis.
Nutrition has been increasingly recognized for its use in mental health. Depression is commonly observed in patients with chronic liver disease (CLD). Building on our recent findings of depression-like behaviors in mice with hepatic ischemia/reperfusion (HI/R) injury, mediated by the gut-liver-brain axis, this study explored the potential influence of dietary sulforaphane glucosinolate (SGS) on these behaviors. Behavioral assessments for depression-like behaviors were conducted 7 days post either sham or HI/R injury surgery. Dietary intake of SGS significantly prevented splenomegaly, systemic inflammation, depression-like behaviors, and downregulation of synaptic proteins in the prefrontal cortex (PFC) of HI/R-injured mice. Through 16S rRNA analysis and untargeted metabolomic analyses, distinct bacterial profiles and metabolites were identified between control + HI/R group and SGS + HI/R group. Correlations were observed between the relative abundance of gut microbiota and both behavioral outcomes and blood metabolites. These findings suggest that SGS intake could mitigate depression-like phenotypes in mice with HI/R injury, potentially through the gut-liver-brain axis. Additionally, SGS, found in crucial vegetables like broccoli, could offer prophylactic nutritional benefits for depression in patients with CLD.
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Cryptotanshinone regulates gut microbiota and PI3K-AKT pathway in rats to alleviate CUMS induced depressive symptoms.
Cryptotanshinone (CPT), a bioactive compound derived from the traditional Chinese herb Salvia miltiorrhiza, exhibits promising antidepressant properties. Employing a rat model subjected to Chronic Unpredictable Mild Stress (CUMS), behavioral analyses (open field experiment, elevated cross maze experiment, sugar water preference experiment, forced swimming experiment) and inflammatory factor assessments were conducted to assess the efficacy of CPT in alleviating depressive symptoms and inflammatory responses induced by CUMS. Moreover, 16 S rDNA analysis revealed alterations in the gut microbiota of rats exposed to both CUMS and CPT administration. Notably, CPT administration was found to mitigate harmful bacterial shifts associated with depression. Preliminary exploration of the molecular mechanism underlying CPT's antidepressant effects via transcriptomics analysis and molecular docking indicated that CPT might exert its influence by regulating the PI3K-AKT pathway. This study sheds light on the potential therapeutic role of CPT in managing depressive disorders, offering a comprehensive understanding of its impact on behavior, inflammation, gut microbiota, and molecular pathways.
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Expression of concern: Ingestion of Bifidobacterium longum subspecies infantis strain CCFM687 regulated emotional behavior and the central BDNF pathway in chronic stress-induced depressive mice through reshaping the gut microbiota.
Expression of concern for 'Ingestion of Bifidobacterium longum subspecies infantis strain CCFM687 regulated emotional behavior and the central BDNF pathway in chronic stress-induced depressive mice through reshaping the gut microbiota' by Peijun Tian et al., Food Funct., 2019, 10, 7588-7598, https://doi.org/10.1039/C9FO01630A.