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Jasmine tea extract prevents CUMS-induced depression-like behaviors through the modulation of microbiota-gut-brain axis.
Depression is strongly linked to dysfunctions in the microbiota-gut-brain axis. Jasmine tea, a traditional Chinese beverage made by combining green tea with Jasminum sambac, has potential antidepressant effects. However, its potential to alleviate depression via modulation of the microbiota-gut-brain axis remains largely unstudied. In this study, we used a rat model of depression induced by chronic unpredictable mild stress (CUMS) to investigate the effects of jasmine tea extract (JT) on depression-related symptoms. Behavioral assessments, inflammatory marker analysis, hippocampal histology, and brain-derived neurotrophic factor (BDNF) expression assays demonstrated that JT alleviated depressive behaviors, reduced brain tissue damage, and restored cognitive function in CUMS-exposed rats. JT also significantly reduced intestinal levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and modulated oxidative stress markers (MDA, SOD, and CAT), suggesting a role in preserving intestinal integrity. Further, 16S rRNA sequencing revealed that JT shifted the gut microbiota composition in favor of beneficial bacteria such as Romboutsia, Blautia, and Monoglobus, while decreasing the abundance of potentially harmful bacteria, including Bifidobacterium, Clostridium_sensu_stricto_1, and Escherichia-Shigella. Meanwhile, non-targeted and targeted metabolomics analyses showed that JT influenced key metabolic pathways involving tryptophan, short-chain fatty acids, and bile acids, helping to restore metabolic balance across various tissues (feces, colon, serum, and cerebral cortex) in the depressed rats. These findings indicate that JT may alleviate depression by modulating the microbiota-gut-brain axis, highlighting its potential as a dietary intervention for depression management.
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Coprococcus eutactus screened from healthy adolescent attenuates chronic restraint stress-induced depression-like changes in adolescent mice: Potential roles in the microbiome and neurotransmitter modulation.
The onset of depression commonly occurs in adolescence; therefore, depressive prevention and intervention are pivotal during this period. It is becoming evident that neurotransmitter imbalance and gut microbiota dysbiosis are prominent causes of depression. However, the underlying links and mechanisms remain poorly understood. In this study, with 16S ribosomal RNA gene sequencing, genus Coprococcus markedly differentiated between the healthy and unmedicated depressive adolescents. Based on this, transplantation of Coprococcus eutactus (C.e.) was found to dramatically ameliorate the chronic restraint stress (CRS) induced depression-like changes and prevent synaptic loss and glial-stimulated neuroinflammation in mice. The Ultra-high performance liquid chromatography tandem mass spectrometry analysis (UHPLC-MS/MS) further showed that neurotoxic neurotransmitters in kynurenine pathway (KP) such as 3-hydroxykynurenine (3-HK) and 3-hydroxyanthranilic acid (3-HAA) decreased in mouse brains, mechanistically deciphering the transfer of the tryptophan metabolic pathway to serotonin metabolic signaling in the brain after C.e. treatment, which was also verified in the colon. Molecularly, blockage of KP activities mediated by C.e. was ascribed to the restraint of the limit-step enzymes responsible for kynurenine, 3-HK, and quinolinic acid generation. In the colon, C.e. treatment significantly recovered goblet cells and mucus secretion in CRS mice which may ascribe to the rebalance of the disordered gut microbiota, especially Akkermansia, Roseburia, Rikenella, Blautia, and Alloprevotella. Taken together, the current study reveals for the first time the beneficial effects and potential mechanisms of C.e. in ameliorating CRS-induced depression, unraveling the direct links between C.e. treatment and neurotransmitter rebalance, which may provide efficacious therapeutic avenues for adolescent depressive intervention.
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Zuojin Pill ameliorates depression with gastrointestinal dysfunction via Parabacteroides distasonis.
BACKGROUND: Brain-gut interaction disorders, such as functional dyspepsia (FD) comorbid with depression, are highly prevalent and severely affect patients' quality of life; however, the underlying mechanisms remain incompletely understood, and effective therapeutic options are still limited. Zuojin Pill (ZJP), a classic Chinese herbal formula, has shown potential in treating both gastrointestinal disorders and depressive symptoms, but its role in FD-depression comorbidity and underlying mechanisms remain unclear. PURPOSE: This investigation aimed to evaluate the therapeutic potential of ZJP and delineate its mechanistic pathways in alleviating comorbid depressive symptoms and Gastrointestinal (GI) impairments. STUDY DESIGN: A combined clinical observational study and preclinical experimental study was conducted to integrate human and animal data for mechanistic validation. METHODS: Baseline assessments were conducted in healthy controls and patients with functional dyspepsia (FD)-depression comorbidity, including evaluations of gut microbiota composition, metabolite profiles, inflammatory cytokines, gastrointestinal hormones, and serotonin (5-HT) levels. An animal model using mice was developed to assess the efficacy of ZJP in addressing depression-related phenotypes and GI functional deficits. Furthermore, Parabacteroides distasonis was used to induce pathological features in mice, and the intervention effects of ZJP were systematically assessed. RESULTS: Patients with FD-depression comorbidity exhibited gut microbiota dysbiosis, characterized by a significant increase in P. distasonis abundance. Metabolomic analysis highlighted tryptophan metabolism as a key altered pathway. In model mice, ZJP administration alleviated depression-like behaviors and gastrointestinal dysfunction. Mechanistically, ZJP targeted P. distasonis, regulated tryptophan-derived metabolites, enhanced anti-inflammatory cytokine expression, improved synaptic plasticity, and restored intestinal mucosal barrier integrity. CONCLUSIONS: ZJP ameliorates depression with gastrointestinal dysfunction by modulating P. distasonis and its associated tryptophan metabolic pathway, thereby restoring gut-brain axis homeostasis. These results establish a mechanistic foundation supporting the therapeutic use of ZJP in treating brain-gut interaction disorders.
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The Microbiome-Gut-Brain Axis in Health and Disease.
Gut microbes are capable of producing most neurotransmitters found in the human brain. Evidence is accumulating to support the view that gut microbes influence central neurochemistry and behavior. Irritable bowel syndrome is regarded as the prototypic disorder of the brain-gut-microbiota axis that can be responsive to probiotic therapy. Translational studies indicate that certain bacteria may have an impact on stress responses and cognitive functioning. Manipulating the gut microbiota with psychobiotics, prebiotics, or even antibiotics offers a novel approach to altering brain function and treating gut-brain axis disorders, such as depression and autism.
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Prenatal metal exposures and childhood gut microbial signatures are associated with depression score in late childhood.
BACKGROUND: Childhood depression is a major public health issue worldwide. Previous studies have linked both prenatal metal exposures and the gut microbiome to depression in children. However, few, if any, have studied their interacting effect in specific subgroups of children. OBJECTIVES: Using an interpretable machine-learning method, this study investigates whether children with specific combinations of prenatal metals and childhood microbial signatures (cliques or groups of metals and microbes) were more likely to have higher depression scores at 9-11 years of age. METHODS: We leveraged data from a well-characterized pediatric longitudinal birth cohort in Mexico City and its microbiome substudy (n = 112). Eleven metal exposures were measured in maternal whole blood samples in the second and third trimesters of pregnancy. The gut microbial abundances were measured at 9-11-year-olds using shotgun metagenomic sequencing. Depression symptoms were assessed using the Child Depression Index (CDI) t-scores at 9-11 years of age. We used Microbial and Chemical Exposure Analysis (MiCxA), which combines interpretable machine-learning into a regression framework to identify and estimate joint associations of metal-microbial cliques in specific subgroups. Analyses were adjusted for relevant covariates. RESULTS: We identified a subgroup of children (11.6 % of the sample) characterized by a four-component metal-microbial clique that had a significantly high depression score (15.4 % higher than the rest) in late childhood. This metal-microbial clique consisted of high Zinc in the second trimester, low Cobalt in the third trimester, a high abundance of Bacteroides fragilis, a high abundance of Faecalibacterium prausnitzii. All combinations of cliques (two-, three-, and four-components) were significantly associated with increased log-transformed t-scored CDI (β = 0.14, 95%CI = [0.05,0.23], P < 0.01 for the four-component clique). SIGNIFICANCE: This study offers a new approach to chemical-microbial analysis and a novel demonstration that children with specific gut microbiome cliques and metal exposures during pregnancy may have a higher likelihood of elevated depression scores.
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Neoagaro-Oligosaccharides Ameliorate Chronic Restraint Stress-Induced Depression by Increasing 5-HT and BDNF in the Brain and Remodeling the Gut Microbiota of Mice.
Neoagaro-oligosaccharides (NAOs) belong to the algae oligosaccharides. NAOs have been found to have diverse biological activities. However, the effects of NAOs on depression and their underlying mechanism have not been thoroughly studied. A chronic restraint stress (CRS)-induced C57BL/6J mouse model was used to assess the antidepressant effects of NAOs. Anxiety and depression behaviors were assessed by open field tests (OFT) and forced swimming tests (FST), while interleukin 18 (IL-18), 5-hydroxytryptamine (5-HT) and brain-derived neurotrophic factor (BDNF) were the molecular biomarkers of depression. Fecal microbiota transplantation (FMT) was performed. The results showed that NAO treatment significantly improved the body weight of depressed mice and reduced the central area time in the OFT and immobility time in the FST. NAO treatment decreased the levels of IL-18 in the serum and increased the levels of 5-HT in the serum and whole brain and of BDNF in the whole brain. NAO treatment mitigated the gut microbiota dysbiosis in the depressed mice and reversed the decreased levels of short-chain fatty acids (SCFAs) in the cecum of the depressed mice. FMT indicated that the gut microbiota is, indeed, linked to depression, which was reflected in the changes in weight gain and behaviors. In a word, NAOs effectively reversed the CRS-induced mice model of depression, which depended on the changes in the gut microbiota and SCFAs, as well as its modulation of 5-HT and BDNF.
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Pathogenesis and potential therapies for perimenopausal depression: Insights from the estrogen-gut microbiota axis.
Perimenopause represents a critical phase during which women are particularly susceptible to depression. Although fluctuations in estrogen levels resulting from ovarian aging and imbalances in the gut microbiota have been identified as contributing factors to the onset of depression, the interplay among these elements is frequently overlooked. Fluctuations in estrogen levels can further influence neurogenesis or apoptosis through effects on neurotransmitter balance, neuroinflammation, neuroendocrine regulation, and mitochondrial function. Meanwhile, dramatic shifts in estrogen levels can diminish microbial diversity and stability, thereby disrupting the homeostasis of metabolites and neurotransmitters via the gut-brain axis (GBA). Such disturbances may induce neuroinflammation, potentially leading to or exacerbating depressive symptoms. Additionally, the estrobolome (gut bacterial genes encoding estrogen-metabolizing enzymes) plays a regulatory role in the reabsorption, excretion, and systemic levels of estrogen through the modulation of β-glucuronidase activity, thereby affecting estrogen homeostasis. This review first examines the influence of fluctuations in estrogen levels on the composition and function of the gut microbiota, as well as the role of the gut microbiota in estrogen metabolism. It then discusses how estrogen deficiency and dysbiosis of the gut microbiota contribute to the pathogenesis of perimenopausal depression, discussing the potential for a vicious cycle mediated by the estrogen-gut microbiota axis that increases susceptibility to this condition. Finally, this review presents bioactive compounds derived from dietary sources or medicinal plants that exhibit estrogenic and prebiotic properties, which may offer diverse strategies for the prevention and management of perimenopausal depression through modulation of the estrogen-gut microbiota axis.
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Behavioural and neurochemical consequences of chronic gut microbiota depletion during adulthood in the rat.
Gut microbiota colonization is a key event for host physiology that occurs early in life. Disruption of this process leads to altered brain development which ultimately manifests as changes in brain function and behaviour in adulthood. Studies using germ-free (GF) mice highlight the extreme impact on brain health that results from life without commensal microbes. However, the impact of microbiota disturbances occurring in adulthood is less studied. To this end, we depleted the gut microbiota of 10-week-old male SpragueDawley rats via chronic antibiotic treatment. Following this marked, sustained depletion of the gut bacteria, we investigated behavioural and molecular hallmarks of gut-brain communication. Our results reveal that depletion of the gut microbiota during adulthood results in deficits in spatial memory as tested by Morris water maze, decreased visceral sensitivity and a greater display of depressive-like behaviours in the forced swim test. In tandem with these clear behavioural alterations we found changes in altered CNS serotonin concentration along with changes in the mRNA levels of corticotrophin releasing hormone receptor 1 and glucocorticoid receptor. Additionally, we found changes in the expression of brain derived neurotrophic factor (BDNF), a hallmark of altered microbiota-gut-brain axis signalling. In summary, this model of antibiotic-induced depletion of the gut microbiota can be used for future studies interested in the impact of the gut microbiota on host health without the confounding developmental influence of early-life microbial alterations.
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Partially Hydrolyzed Guar Gum Modulates Gut Microbiota, Regulates the Levels of Neurotransmitters, and Prevents CUMS-Induced Depressive-Like Behavior in Mice.
SCOPE: Depression is the leading cause of disability around the world; however, most antidepressants have drug tolerance and serious side effects. In this study, it is explored whether partially hydrolyzed guar gum (PHGG) is a safe food that exhibits protection in a mouse model of depression. METHODS AND RESULTS: PHGG is orally administered to mice with depression induced by chronic unpredictable mild stress (CUMS) in two animal experiments (prevention trial and intervention trial) to characterize the potentially protective effect of PHGG. The results in the prevention trial show that PHGG significantly inhibits the loss of body weight, and prevents CUMS-induced depressive-like behavior in mice. The beneficial effects may be associated with PHGG modulating the gut microbiota structure and then increasing the levels of short-chain fatty acids in mice feces and the levels of 5-hydroxytryptamine and dopamine in serum, striatum, and hippocampus. Besides, PHGG in the intervention trial is less effective than that in the prevention trial, but it may have a synergistic effect on improving depression with fluoxetine. CONCLUSIONS: This study suggests that moderate daily intake of PHGG can contribute to relieving depressive-like behavior.
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Parabacteroides distasonis in depression: Triggers or outcomes.