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Electroacupuncture Alleviates Comorbid Depression-Like Behaviors and Dyspepsia-Like Symptoms in Rats Accompanied by Alterations in Hippocampal Neuroinflammation and Gut Microbiota.
BACKGROUND: Depression and dyspepsia are highly comorbid in clinical practice, and their occurrence and progression are closely associated with dysfunction of the brain-gut axis. Electroacupuncture (EA) can improve depression and gastrointestinal dysfunction at the same time. However, whether its therapeutic effects are mediated through regulation of the brain-gut axis remains unclear. METHODS: We established a rat model of comorbid depression-like and dyspepsia-like symptoms using SD rats. Behavioral tests were used to evaluate anxiety- and depression-like states in rats. Gastric emptying rate, small intestinal propulsion rate, and gastrointestinal hormones were measured to assess gastrointestinal motility. Histomorphological changes in the hippocampus, stomach, and duodenum were observed by hematoxylin-eosin (HE) staining and Nissl staining. Immunofluorescence (IF), Western blotting, quantitative real-time polymerase chain reaction (RT-qPCR), and biochemical assays were used to determine the activation status of hippocampal microglia and mitochondrial reactive oxygen species (mtROS)/NOD-like receptor family pyrin domain containing 3 (mtROS/NLRP3) pathway-related indicators. Enzyme-linked immunosorbent assay was used to determine central and peripheral levels of 5-hydroxytryptamine (5-HT) and inflammatory factors. Gut microbiota diversity and composition were analyzed by 16S rRNA sequencing. The expression of duodenal mucosal barrier-related proteins was detected by immunofluorescence, and the ultrastructure of the duodenum was observed by transmission electron microscopy. RESULTS: EA significantly alleviated anxiety- and depression-like behaviors and improved gastrointestinal motility in model rats. EA ameliorated hippocampal neuronal injury, increased Nissl body number, reduced mtROS and malondialdehyde levels, enhanced mitochondrial membrane potential and superoxide dismutase activity, and suppressed microglial activation and NLRP3 inflammasome signaling. In addition, EA increased central and peripheral 5-HT levels while decreasing Interleukin-6 (IL-6) and tumor necrosis factor-α expression. EA also modulated gut microbiota composition by reducing opportunistic pathogens and enriching beneficial bacteria. Moreover, EA improved duodenal ultrastructure and upregulated the tight junction proteins ZO-1 and Occludin. CONCLUSION: EA can improve depression-like behaviors and dyspepsia-like symptoms in comorbid rats. These behavioral and gastrointestinal improvements were accompanied by reduced hippocampal oxidative stress and neuroinflammation, altered gut microbiota composition, and improved duodenal mucosal barrier. These findings suggest that the therapeutic mechanism of EA may involve regulation of the brain-gut axis, although the specific causal relationships among its individual components remain to be elucidated.
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A combination of potential psychobiotics alleviates anxiety and depression behaviors induced by chronic unpredictable mild stress.
Strains of Roseburia inulinivorans, Bacteroides uniformis, and Eubacterium rectale have exhibited multi-pathway therapeutic efficacy against anxiety and depression-like behaviors in chronic unpredictable mild stress (CUMS) rats. However, the combined therapeutic effects of these strains remain to be elucidated. Behavioral tests showed that a mixture of these strains reduced anxiety and depression-like behaviors. 16S rRNA sequencing revealed that the mixtures decrease the relative abundance of potentially pathogenic bacteria within the gut microbiota. Furthermore, the mixture increased the levels of butyric, isobutyric, and isovaleric acids in the gut and decreased pro-inflammatory factors in serum. It also lowered diamine oxidase, histamine in brain tissue, increased DL-kynurenine, and reduced cortisol secretion by the hypothalamic pituitary adrenal axis. In summary, the mixture significantly alleviated anxiety and depression-like behaviors.
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Global research trends in the intestinal microflora and depression: bibliometrics and visual analysis.
BACKGROUND: In recent years, the relationship between gut microbiota and human health has garnered significant attention. Notably, the potential connection between gut microbiota and mental health issues, such as depression and anxiety, has emerged as a new focal point for research. While some studies suggest a possible link between these factors, the field remains in its early stages of development, and there are notable methodological and sample size limitations. PURPOSE: This study aims to systematically summarize the knowledge systems, research hotspots, and development trends related to intestinal microflora within the context of depression research. METHODS: This study conducted a search for publications related to intestinal microflora and depression in the Web of Science Core Collection (WOSCC) prior to August 6, 2024. The selected literature was subsequently analyzed using VOSviewer (v.1.6.20), SCImago Graphica (v.1.0.39), and CiteSpace (v.6.3.1). RESULTS: The study encompassed a total of 1,046 publications, demonstrating a consistent increase in annual publication volume. The primary research countries identified are China and the United States, with notable contributions from institutions such as the University of California and University College Cork, among others. Keywords analysis highlighted high-frequency terms including "gut microbiota," "depression," and "anxiety," and revealed 10 keyword clusters along with 20 strongest citation bursts keywords. The focus of research has shifted from compositional analysis of gut microbiota to its role in the pathogenesis of depression. CONCLUSIONS: Research on gut microbiota and depression is growing, but there is still a need for greater collaboration between authors and institutions across regions, more ongoing interaction and communication to further explore the mechanisms of action of gut microbiota, to develop microbiota-based interventions, and to facilitate translation of research findings into clinical practice.
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Food and mood: how do diet and nutrition affect mental wellbeing?
Poor nutrition may be a causal factor in the experience of low mood, and improving diet may help to protect not only the physical health but also the mental health of the population, say Joseph Firth and colleagues
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Prevalence of perturbed gut microbiota in pathophysiology of arsenic-induced anxiety- and depression-like behaviour in mice.
Severe toxic effects of arsenic on human physiology have been of immense concern worldwide. Arsenic causes irrevocable structural and functional disruption of tissues, leading to major diseases in chronically exposed individuals. However, it is yet to be resolved whether the effects result from direct deposition and persistence of arsenic in tissues, or via activation of indirect signaling components. Emerging evidences suggest that gut inhabitants play an active role in orchestrating various aspects of brain physiology, as the gut-brain axis maintains cognitive health, emotions, learning and memory skills. Arsenic-induced dysbiosis may consequentially evoke neurotoxicity, eventually leading to anxiety and depression. To delineate the mechanism of action, mice were exposed to different concentrations of arsenic. Enrichment of Gram-negative bacteria and compromised barrier integrity of the gut enhanced lipopolysaccharide (LPS) level in the bloodstream, which in turn elicited systemic inflammation. Subsequent alterations in neurotransmitter levels, microglial activation and histoarchitectural disruption in brain triggered onset of anxiety- and depression-like behaviour in a dose-dependent manner. Finally, to confirm whether the neurotoxic effects are specifically a consequence of modulation of gut microbiota (GM) by arsenic and not arsenic accumulation in the brain, fecal microbiota transplantations (FMT) were performed from arsenic-exposed mice to healthy recipients. 16S rRNA gene sequencing indicated major alterations in GM population in FMT mice, leading to severe structural, functional and behavioural alterations. Moreover, suppression of Toll-like receptor 4 (TLR4) using vivo-morpholino oligomers (VMO) indicated restoration of the altered parameters towards normalcy in FMT mice, confirming direct involvement of the GM in inducing neurotoxicity through the arsenic-gut-brain axis. This study accentuates the potential role of the gut microbiota in promoting neurotoxicity in arsenic-exposed mice, and has immense relevance in predicting neurotoxicity under altered conditions of the gut for designing therapeutic interventions that will target gut dysbiosis to attenuate arsenic-mediated neurotoxicity.
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A distinct plasma lipidomic signature and multi-omics network in depression of polycystic ovary syndrome.
Patients with polycystic ovary syndrome (PCOS) are at an elevated risk of depression, yet the underlying mechanisms remain elusive. Emerging evidence implicates the gut-brain axis and systemic lipid homeostasis alterations as potential key contributors. We profiled untargeted plasma lipidomes of PCOS patients with and without comorbid depression (PCOS-DP) and integrated these data with our prior gut microbial and host transcriptomic datasets to construct multi-omics interaction networks. The causal role of the candidate gut microbial was preliminary explored in a germ-free PCOS mouse model using fecal microbiota transplantation, followed by behavioral phenotyping and ELISA-based protein quantification. We identified a distinct plasma lipidomic signature differentiating PCOS-DP from PCOS alone, characterized primarily by the downregulation of 26 lipid species. Most of these altered lipids were triacylglycerols (TAGs) enriched with FA18:1 and FA18:2, whose levels correlated with coagulation dysfunction. Multi-omics network analysis revealed significant interconnections between depression-associated gut microbiota (including Bacteroides eggerthii), specific altered lipids such as TAG (60:12/FA22:6), and host genes involved in inflammation (e.g., IL22, NLRP7), metabolism, and neural processes. Animal validation demonstrated that B. eggerthii colonization in PCOS mice specifically exacerbated anhedonia and hyperlocomotion, alongside modulating plasma IL-22 expression, suggesting its context-dependent neurobehavioral effect role. This study delineates a TAG-downregulated lipid signature with diagnostic potential and reveals a novel "gut microbiota-lipid-host gene" interaction network underpinning PCOS-DP, with B. eggerthii as a key microbial modulator of neurobehavioral phenotypes in the context of PCOS. These findings provide new pathophysiological insights and highlights potential diagnostic biomarkers for PCOS-DP.
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Lactobacillus casei improves depression-like behavior in chronic unpredictable mild stress-induced rats by the BDNF-TrkB signal pathway and the intestinal microbiota.
Lactobacillus casei (L. casei), a kind of probiotics, is known as a "healthy triple benefit bacterium" along with Lactobacillus acidophilus and Bifidobacterium. L. casei is associated with the alteration of the intestinal flora population, and the gut microbiota-brain axis has been demonstrated to play an important role in many central nervous system diseases. The aim of this study was to evaluate the effectiveness of L. casei intervention in ameliorating mental disorders and potential mechanisms using a rat model with depression-like behaviour induced by chronic unpredictable mild stress (CUMS). L. casei intervention improved the CUMS-induced depression-like behaviors of rats, including a reduced body growth rate, decreased sucrose preference, increased immobility time, and lowered moving distance and velocity. In addition, L. casei intervention amended the gut microbiota structure changes induced by CUMS in rats. Furthermore, L. casei intervention reversed the CUMS-induced protein expression changes of monoamines dopamine, noradrenaline and 5-hydroxytryptamine, brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase receptor B (TrkB), and N-methyl-d-aspartic acid receptor 1, as well as CUMS-induced activations of ERK1/2 and p38 MAPK signal pathways. These findings suggested that L. casei could significantly protect against depression in rats, which was possibly associated with the alterations in the gut microbiota composition and mediation of BDNF-TrkB signaling.
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Liqi Yangyin formula ameliorates CUMS-induced depression and comorbid constipation via ACE/FFAR2 modulation of the microbiota-gut-brain axis.
BACKGROUND: The gut-brain axis, involving bidirectional signaling between the gastrointestinal tract and the central nervous system. Clinical observations have shown that Liqi Yangyin (LQYY) can effectively relieve symptoms of depression accompanied by constipation. However, whether LQYY exerts its effects through gut-brain crosstalk remains to be elucidated. METHODS: A chronic unpredictable mild stress (CUMS) protocol was employed to establish a mouse model. H&E and Nissl staining were used to examine pathological changes in the prefrontal cortex (PFC) and colon. The ultrastructure of the intestinal barrier was observed via transmission electron microscopy, while the expression of the blood-brain barrier tight junction proteins was quantified by Western blotting (WB). ELISA quantified inflammatory factors and serotonin (5-HT) levels. Immunohistochemistry, immunofluorescence, and WB analyzed IBA-1 and Free fatty acid receptor 2 (FFAR2) expression levels. Gut microbiota composition was analyzed via 16S rDNA sequencing, and SCFAs levels were quantified using UHPLC-TSQ Altis Plus. Additionally, in vitro studies using BV-2 cells involved treatments with acetic acid (ACE) and an FFAR2 antagonist, after which the expression of relevant indicators was assessed. RESULTS: Our results demonstrated that LQYY significantly ameliorated CUMS-induced behavioral changes and improved intestinal motility. These effects were associated with the restoration of gut microbiota balance and an increase in ACE levels. LQYY increased FFAR2 expression, leading to reduced neuroinflammation and enhanced colonic 5-HT secretion. Furthermore, LQYY protected intestinal and blood-brain barrier integrity and improved neuronal morphology in the PFC. In vitro studies confirmed that ACE suppresses microglial inflammation through upregulating FFAR2 expression, an effect that was attenuated by the FFAR2 inhibitor GLPG0974. CONCLUSIONS: These findings suggest that LQYY modulates the gut-brain axis through ACE/FFAR2, offering a promising therapeutic approach for depression and constipation.
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A key role of the subdiaphragmatic vagus nerve in the depression-like phenotype and abnormal composition of gut microbiota in mice after lipopolysaccharide administration.
The vagus nerve plays a role in the cross talk between the brain and gut microbiota, which could be involved in depression. The subdiaphragmatic vagus nerve serves as a major modulatory pathway between the brain and gut microbiota. Here, we investigated the effects of subdiaphragmatic vagotomy (SDV) on the depression-like phenotype and the abnormal composition of gut microbiota in mice after lipopolysaccharide (LPS) administration. LPS caused a depression-like phenotype, inflammation, increase in spleen weight, and downregulation of synaptic proteins in the medial prefrontal cortex (mPFC) in the sham-operated mice. In contrast, LPS did not produce a depression-like phenotype and downregulated synaptic proteins in the mPFC after SDV. The spleen weight and plasma levels of pro-inflammatory cytokines in the SDV + LPS group were lower than those of the sham + LPS group. Interestingly, there were positive correlations between the plasma levels of pro-inflammatory cytokines and spleen weight, suggesting a relationship between inflammatory events and spleen weight. Furthermore, LPS led to significant alterations in gut microbiota diversity in sham-operated mice, but not SDV-operated mice. In an unweighted UniFrac PCoA, the dots representing the sham + LPS group were located far away from the dots representing the other three groups. Our results suggest that LPS produces a depression-like phenotype, increases spleen weight, triggers inflammation, downregulates synaptic proteins in the mPFC, and leads to abnormal composition of gut microbiota via the subdiaphragmatic vagus nerve. It is likely that the vagus nerve plays a crucial role in the brain-gut-microbiota axis.
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Interrogating the Gut-Brain Axis in the Context of Inflammatory Bowel Disease: A Translational Approach.
This review examines preclinical and clinical studies relevant to our understanding of how the bidirectional gut-brain axis influences the natural history of inflammatory bowel disease. Preclinical studies provide proof of concept that preexisting behavioral illness, such as depression, results in increased susceptibility to inflammatory stimuli and that commonly used classes of antidepressants protect against this vulnerability. However, clinical studies suggesting behavioral illness as a risk factor for IBD and a protective role for antidepressants have relied primarily on symptom-reporting rather than objective measurements of inflammation. In terms of gut-to-brain signaling, there is emerging evidence from preclinical and clinical observation that intestinal inflammation alters brain functions, including the induction of mood disorders, alteration of circadian rhythm both centrally and peripherally, and changes in appetitive behaviors. Furthermore, preclinical studies suggest that effective treatment of intestinal inflammation improves associated behavioral impairment. Taken together, the findings of this review encourage a holistic approach to the management of patients with IBD, accommodating lifestyle issues that include the avoidance of sleep deprivation, optimized nutrition, and the monitoring and appropriate management of behavioral disorders. The review also acknowledges the need for better-designed clinical studies evaluating the impact of behavioral disorders and their treatments on the natural history of IBD, utilizing hard end points to assess changes in the inflammatory process as opposed to reliance on symptom-based assessments. The findings of the review also encourage a better understanding of changes in brain function and circadian rhythm induced by intestinal inflammation.