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[Antidepressant effects of Ziziphi Spinosae Semen extract on depressive-like behaviors in sleep deprivation rats based on integrated serum metabolomics and gut microbiota].
Based on serum metabolomics and gut microbiota technology, this study explores the effects and mechanisms of the water extract of Ziziphi Spinosae Semen(SZRW) and the petroleum ether extract of Ziziphi Spinosae Semen(SZRO) in improving depressive-like behaviors induced by sleep deprivation. A modified multi-platform water environment method was employed to establish a rat model of sleep deprivation. Depressive-like behaviors in rats were assessed through the sucrose preference test and forced swim test. The expression of barrier proteins, such as Occludin, in the colon was determined by immunofluorescence. UPLC-Q-Orbitrap MS was utilized to analyze the serum metabolic profiles of sleep-deprived rats, screen for differential metabolites, and analyze metabolic pathways. The diversity of the gut microbiota was detected using 16S rRNA gene sequencing. Spearman correlation coefficient analysis was conducted to assess the correlation between differential metabolites and gut microbiota. The results indicated that SZRO significantly increased the sucrose preference index and decreased the immobility time in the forced swim test in rats. A total of 34 differential metabolites were identified through serum metabolomics. SZRW and SZRO shared five metabolic pathways, including phenylalanine metabolism. SZRW uniquely featured taurine and hypotaurine metabolism, while SZRO uniquely featured linoleic acid metabolism and tyrosine metabolism. Correlation analysis revealed that SZRW could upregulate the abundance of Bilophila, promoting the production of indole-3-propionic acid and subsequently upregulating the expression levels of intestinal tight junction proteins such as ZO-1, Occludin, and Claudin-1. SZRO could indirectly influence metabolic pathways such as arginine metabolism and linoleic acid metabolism by upregulating the abundance of gut microbiota such as Coprococcus and Eubacterium species. Both SZRW and SZRO can regulate endogenous metabolism, including amino acids, energy, and lipids, alter the gut microbiota microecology, and improve depressive-like behaviors. SZRO demonstrated superior effects in regulating metabolic pathways and gut microbiota structure compared to SZRW. The findings of this study provide a scientific basis for elucidating the pharmacodynamic material basis of Ziziphi Spinosae Semen.
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A study on the differences in the gut microbiota and metabolism between male and female mice in different stress periods.
The sex difference in depression has long been an unsolved issue. Women are twice as likely to suffer from depression as men. However, there were significant differences in the composition of gut microbiota between women and men. There is a lack of studies linking sex differences in depression to microbiota, and the specific mechanisms of this process have not been explained in detail. The main purpose of this study was to explore the gender differences in the intestinal tract of male and female depressed mice. In this study, chronic restraint stress (CRS) mouse models were used to simulate chronic stress, and behavioral tests were conducted, including the open field test (OFT), tail suspension test (TST) and forced swimming test (FST). Microbial diversity analysis and metabolomics were performed on collected mouse feces. The results showed that female mice were highly active and prone to anxious behavior before stress, and the levels of f-Rikenellaceae, f-Ruminococcaceae and 16α-hydroxyestrone were significantly different from those in male mice. After 21 days (Days) of stress, female mice showed depression-like behavior, and the levels of f-Erysipelotrichaceae, 5α-pregnane-3,20-dione, and 2-hydroxyestradiol were significantly different from those in male mice. After 14 days of stress withdrawal, the depression-like behavior continued to worsen in female mice, and the levels of 5α-pregnane-3,20-dione, estrone glucuronide and f-Erysipelotrichaceae were significantly different from those in male mice. In summary, female mice have stronger stress sensitivity and weaker resilience than male mice, which may be related to differences in bacterial diversity and estrogen metabolism disorders.
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From gut inflammation to psychiatric comorbidity: mechanisms and therapies for anxiety and depression in inflammatory bowel disease.
Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), is characterized by complex aetiological factors and extensive extraintestinal manifestations. Anxiety and depression, which are common mental disorders, have shown increasing incidence rates in recent years. Compared with the general population, IBD patients are more susceptible to anxiety and depression, which consequently exacerbate the disease burden and increases the risk of adverse clinical outcomes. Emerging evidence reveals shared pathophysiological mechanisms between IBD and anxiety and depression. This review rigorously focuses on anxiety and depression in IBD, distinguishing these conditions from primary anxiety or depressive disorders, as well as from mood disturbances secondary to other chronic illnesses, and summarizes the latest research literature highlighting their unique comorbid characteristics. Firstly, we integrate recent epidemiological evidence to establish their bidirectional relationship. Subsequently, we summarize the comorbid mechanisms as follows: genetic predisposition, impaired hippocampal neurogenesis, specific brain region alterations, gut microbiota dysbiosis, hypothalamic‒pituitary‒adrenal (HPA) axis dysregulation and neuroimmune interactions mediated by inflammatory cytokines and neurotransmitters. Finally, we explore novel therapeutic approaches derived from these mechanistic insights, aiming to enhance clinical recognition of this bidirectional comorbidity and optimize the management of such comorbid conditions.
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Reproducible induction of depressive-like behavior in C57BL/6J mice exposed to chronic social defeat stress with a modified sensory contact protocol.
AIMS: C57BL/6J mice are well-known to exhibit resilience to chronic social defeat stress (CSDS) for induction of depressive-like behavior. Establishment of protocols for reproducible induction of depressive-like behavior in C57BL/6J mice would be useful to elucidate the underlying molecular mechanisms using target gene-knock-in and -out mice whose background is generally C57BL/6J. Here, we developed a modified CSDS protocol for reproducible induction of depressive-like behavior in C57BL/6J mice, and compared the profile of their gut microbiota with that with the standard CSDS protocol. MAIN METHODS: To prevent acclimation of defeated C57BL/6J mice to aggressive ICR mice, the sensory contact following a daily 10 min-defeat episode was performed by housing an individual defeated mouse in a cage set next to a cage for the aggressor one. KEY FINDINGS: The number of attacks by ICR mice on C57BL/6J ones was significantly increased with the modified CSDS protocol, and the susceptible mice exhibited greater hippocampal inflammation and an increased immobility time in the forced swim test, compared in the case of the standard CSDS protocol, and the reproducibility was confirmed in another set of experiments. Both the standard and modified CSDS protocols changed the diversity and relative composition of gut microbiota in the susceptible mice, but there was no apparent difference in them between the standard and modified CSDS-susceptible mice. SIGNIFICANCE: We established a CSDS protocol for reproducible induction of depressive-like behavior in C57BL/6J mice, and the features of the gut microbiota were similar in the susceptible mice with and without the depressive-like behavior.
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Gut microbiota, circadian rhythms and their interactions: implications for the pathogenesis and treatment of depression.
BACKGROUND: Depression is a complex and widespread mental illness that remains poorly understood in terms of pathogenesis and treatment. Recent research has highlighted the intricate connections between gut microbiota and circadian rhythms and indicated that they may serve as significant factors associated with depression. DISCUSSION: The gut microbiota and its metabolites may affect circadian rhythms via microbial oscillations, neurotransmitters, vagus nerve, epigenetic modifications and immune regulation, whereas the circadian rhythms may affect the gut microbiota via circadian gene expression, neurotransmitters, vagus nerve and immune regulation. These findings may provide new perspectives on the pathogenesis of depression and have led to the development of novel treatments targeting the gut microbiota, circadian rhythms and their interactions. This review explores how disturbances in the gut microbiota and circadian rhythms may contribute to depression and discusses the innovative treatments that have resulted from this knowledge. CONCLUSION: By focusing on this emerging area of study, this review reveals promising new developments in the pathogenesis and treatment of depression, emphasizing the novel concept that balancing our internal microbiome and body clock could be key to effectively managing this condition.
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Probiotic L. reuteri treatment in stressed rats improves maternal care and corrects corticosterone-BDNF-oxytocin balance offering insights for maternal postpartum distress treatment.
Mothers experiencing depressive symptoms or gestational stress are at risk of developing maternal distress, which, in its most severe form, can progress to postpartum depression, profoundly affecting maternal well-being and infant care. Using a late-gestation restraint stress model, we investigated whether postpartum treatment of lactating dams with probiotic Limosilactobacillus reuteri (L. reuteri) could reverse stress-induced disruptions in maternal behavior and neurobiology. L. reuteri effectively improved maternal care, and restored reactivity to pup separation in stressed dams. Postpartum L. reuteri also corrected corticosterone-oxytocin imbalances in plasma, normalized hypothalamic oxytocin levels, the unglycosylated and glycosylated oxytocin receptor isoforms and it regulated the ratio of precursor to mature brain-derived neurotrophic factor (BDNF). Additionally, L. reuteri restored gut microbiota balance, increasing Lactobacillus spp. while reducing pathogenic strains in fecal pellets of stressed dams during lactation and post-weaning, correlating with both maternal oxytocin and corticosterone plasma levels. This study is the first to demonstrate the therapeutic efficacy of a probiotic and its molecular support in counteracting the adverse effects of gestational stress on maternal care through brain-gut axis mechanisms. These findings support probiotic-based interventions as safe, complementary preventive strategy for improving maternal health in conditions involving impaired maternal care and microbiota dysbiosis.
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Berberine: An isoquinoline alkaloid targeting the oxidative stress and gut-brain axis in the models of depression.
Depression seriously affects people's quality of life, and there is an urgent need to find novel drugs to cure treatment-resistant depression. Berberine (BBR), extracted from Coptis chinensis Franch., Phellodendron bark, Berberis vulgaris, and Berberis petiolaris, could be a potential multi-target drug for depression. To summarize the effects of BBR on depression in terms of in vitro or in vivo experiments, we searched electronic databases, such as PubMed, Web of Science, Google Scholar, Wanfang Database, and China National Knowledge Infrastructure, from inception until May 2024. Then, we summarize that BBR has indirect antidepressant properties to improve depressive symptoms, manifesting in modulating the gut microbial community, strengthening the intestinal barrier, increasing the abundance of short-chain fatty acid-producing bacteria, and regulating tryptophan metabolism. BBR also exerts antidepressant-like effects via remodulating nuclear factor-erythroid 2-related factor 2/antioxidant response element pathway, hypothalamic-pituitary-adrenal axis, and peroxisome proliferators-activated receptor-delta. Nevertheless, further clinical trials and more high-quality animal studies are needed to show the actual clinical value of BBR for depression.
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Effects of 4G-beta-D-Galactosylsucrose in patients with depression: A randomized, double-blinded, placebo-controlled, parallel-group comparative study.
Advances in genetic research on microbiome have led to several trials on the effectiveness of synbiotics or probiotics in patients with depression; however, none have evaluated the efficacy of prebiotics. 4G-beta-D-Galactosylsucrose (Lactosucrose, LS) is selectively assimilated by Bifidobacterium as a prebiotic and improves microbiome diversity. However, as it is not clear if LS consumption can improve symptoms of depression, we investigated whether LS intake can improve depressive symptoms, quality of life (QOL), and self-efficacy by conducting a single cite, double-blinded, randomized controlled trial in 20 outpatients with depressive episodes (F32, ICD-10) for 24 weeks. Participants (age range, 36-72 years) were randomized to the LS (n = 9) or placebo groups (n = 11). Primary outcome was improvement in total Montgomery Asberg Depression Rating Scale (MADRS) score, and the secondary outcomes were MADRS subscores, global self-efficacy scale (GSES) score, World Health Organization QOL (WHO/QOL-26) score, and 16S rRNA analysis of the fecal microbiome. LS consumption did not significantly improve total MADRS scores (-2 (-16 to 16) vs 0 (-6 to 10), p = 0.552), but GSES tended to improve in the LS group (2.00 ± 4.24 vs -1.36 ± 4.15, p = 0.091) with a large effect size (Cohen's d = 0.802). Sequencing of 16S rRNA revealed individual-level differences in microbiome diversity changes due to the intervention. Thus, we show that LS intake can improve self-efficacy, but not depressive symptoms, even in a small sample. Additional studies that also regulate diet and ensure adherence may help determine a correlation between depression and the gut microbiome.
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Administration time modify the anxiolytic and antidepressant effects of inulin via gut-brain axis.
An imbalance in the microbiota-gut-brain axis exerts an essential effect on the pathophysiology of depressive and anxiety disorders. Our previous research revealed that the timing of inulin administration altered its effects on chronic unpredictable mild stress (CUMS)-induced anxiety and depression. However, it is still unclear if the gut-brain axis is primarily responsible for these effects. In this study, fecal microbiota transplantation (FMT) confirmed that inulin administration at different times alleviated CUMS-induced anxiety- and depression-like behaviors via the gut-brain axis. The time of administration seemed to modify the anxiolytic and antidepressant effects of inulin, and inulin intervention in the evening was more pronounced in inhibiting the inflammatory responses than that of morning inulin intervention. Serum metabolomics analysis showed that the main differential metabolites, including fenofibric acid, 4'-Hydroxyfenoprofen glucuronide and 5-(4-Hydroxybenzyl)thiazolidine-2,4-dione may be vital for the anxiolytic and antidepressant effects of different inulin treatment times. Our results suggested that inulin administration in the evening was more effective in alleviating the inflammatory responses and improving amino acids metabolism. This study provides a new potential link between the microbiota-gut-brain axis and chrono-nutrition, demonstrating that a more appropriate administration time results in a better intervention effect.
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Treatment of male rats with finasteride, an inhibitor of 5alpha-reductase enzyme, induces long-lasting effects on depressive-like behavior, hippocampal neurogenesis, neuroinflammation and gut microbiota composition.
Persistent alteration of plasma neuroactive steroid levels associated with major depression has been recently reported in men after the suspension of the treatment for androgenetic alopecia with finasteride, an inhibitor of the enzyme 5alpha-reductase. Observations in male rats confirmed persistent alterations in neuroactive steroid levels also in the brain. In the present study, we have ascertained possible effects on depressive-like behavior, neurogenesis, gliosis, neuroinflammation and gut microbiota in male rats after subchronic treatment for 20 days with finasteride and after one month of its withdrawal. At the end of treatment there was an increase in the number of pH3 immunoreactive cells in the subgranular zone of the dentate gyrus together with an increase in the mRNA levels of TNF-α in the hippocampus. By one month after the end of finasteride treatment, rats showed depressive-like behavior coupled with a decrease in the number of pH3 immunoreactive cells in the subgranular zone of the dentate gyrus, a decrease in granule cell density in the granule cell layer and an increase in the number of GFAP immunoreactive astrocytes in the dentate gyrus. Finally, alteration of gut microbiota (i.e., an increase in Bacteroidetes phylum and in Prevotellaceae family at the end of the treatment and a decrease in Ruminococcaceae family, Oscillospira and Lachnospira genus at the end of the withdrawal period) was detected. In conclusion, finasteride treatment in male rats has long term effects on depressive-like behavior, hippocampal neurogenesis and neuroinflammation and gut microbiota composition.