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Icariside II Ameliorates Depression Induced by High-Fat Diet via the Microbiota-Gut-Brain Axis in Mice.
Obesity can lead to depression via the microbiota-gut-brain axis. Icariside II (ICS II), a flavonoid compound derived from the traditional Chinese medicine Herbal Epimedium, exerts excellent neuroprotective effects. However, the pharmacological effects and underlying mechanisms of ICS II in obesity-induced depression remain unexplored. The present study aims to investigate whether ICS II can mitigate depression induced by a high-fat diet (HFD) in mice through modulating the microbiota-gut-brain axis. Metabolic parameters were reflected through changes in body weight and blood lipids, while depressive phenotypes were evaluated through behavioral tests and neurotransmitter analysis. The microbiota composition was analyzed by 16S ribosomal RNA gene sequencing, and short chain fatty acids (SCFAs) were detected by liquid chromatography-tandem mass spectrometry. The gut barrier and brain blood barrier (BBB) functions were observed by pathological methods. Fecal microbiota transplantation was used to demonstrate the causality of microbiota-mediated effects. The results showed that ICS II alleviated obesity status and depressive-like behaviors. ICS II reshaped gut microbiota and increased SCFAs. Meanwhile, ICS II relieved gut barrier impairment and systemic inflammation. In the brain, ICS II alleviated neuroinflammation and BBB injury. Intriguingly, fecal microbiota from ICS II-treated HFD mice improved depressive-like behaviors, intestinal barrier dysfunction, and BBB damage compared with those receiving microbiota from HFD mice. Our findings reveal for the first time that ICS II improves the obesity-related metabolic dysregulation and alleviates HFD-induced depression via the microbiota-gut-brain axis. Overall, this study indicates that ICS II is a potential candidate compound for treating obesity-related mental diseases.
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[Modified Chaihu Shugan Powder alleviates cholesterol gallstones in mice with liver depression syndrome by regulating gut microbiota and bile acid metabolism].
OBJECTIVES: To investigate the therapeutic effect of modified Chaihu Shugan San (CHSGS) in mice with cholesterol gallstones (CS) and liver depression syndrome and its potential mechanism. METHODS: Sixty male C57BL/6 mice were randomly divided into blank group (n=9) and model group (n=51) with CS induced by high-lithogenic diet feeding. After verification of successful modeling in 3 mice, the remaining 48 mouse models were divided into CS group, CS-liver depression (CS-LD) group, CHSGS group, and ursodeoxycholic acid (UDCA) group, and the latter 3 groups were subjected to CS-LD modeling by chronic unpredictable mild stress (CUMS) and solitary raising and treated with saline, CHSGS or UDCA gavage for 3 weeks. The mice were assessed for general state, body weight, depressive behavior, ileal pathologies, biliary total cholesterol (TC) and total bile acid (TBA) levels, and ileal mRNA expressions of TGR5, GLP-1, and GLP-2 using q-PCR. 16S rDNA sequencing and metabolomics studies were used to analyze fecal microbiota and bile acids of the mice. RESULTS: Compared to the blank control and CS mice, the CS-LD mouse models showed decreased body weight, depressive behaviors, enlarged gallbladder with crystals, intestinal villi damage, increased biliary TC, decreased TBA, and increased ileal GLP-1/2 and TGR5 mRNA expressions, which were obviously improved by CHSGS treatment. Microbiota analysis revealed decreased alpha diversity in CS and CS-LD groups, with altered abundances of Verrucomicrobiota, Akkermansia, Bacteroidota, and Muribaculaceae. Bile acid profiling revealed significant upregulation of TDCA, DCA, and GDCA in CS group and increased CA and 3-ketodeoxycholic acid levels in CS-LD group. Correlation analysis suggested positive correlations between pro-lithogenic bile acids and the harmful gut bacteria. CONCLUSIONS: Modified CHSGS alleviates liver depression and cholesterol gallstones in mice likely by ameliorating gut microbiota dysbiosis and bile acid metabolism disorders.
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Investigating the modulatory effects of lactoferrin on depressed rats through 16S rDNA gene sequencing and LC-MS metabolomics analysis.
Lactoferrin is a natural multifunctional glycoprotein with potential antidepressant-like effects. However, the mechanism of its antidepressant effect has not been explored from the perspective of gut flora metabolism. Therefore, we employed both 16S rDNA gene sequencing and LC-MS metabolomics analysis to investigate the regulatory effects and mechanisms of lactoferrin in a rat model of depression. After one week of acclimatization, twenty-four 7-week-old male Sprague-Dawley rats were randomly and equally assigned into three groups: the control group, the model group, and the lactoferrin intervention group. The control group rats were housed under standard conditions, while the rats in the model and lactoferrin intervention groups were individually housed and exposed to chronic unpredictable mild stress for 44 days simultaneously. The lactoferrin intervention group was provided with water containing 2% lactoferrin (2 g/100 ml). Behavioural tests were conducted at week 7. Upon completion of the behavioral tests, the rats were anesthetized with isoflurane, humanely euthanized using a rat guillotine, and tissue samples were collected for further experiments. The results indicated that lactoferrin intervention led to an increase in sucrose solution consumption, horizontal movement distance, number of cross platforms, and residence time in the target quadrant. Additionally, it resulted in an increase in jejunal tight junction protein ZO-1 expression and a suppression of serum expression of inflammatory factors, Lipopolysaccharide and Diamine oxidase. In summary, lactoferrin can regulate the metabolic disorder of intestinal flora, reduce intestinal permeability, and further regulate the metabolic balance of hippocampal tissues through the microbiota-gut-brain axis. This process ultimately alleviates the depression-like behavior in rats.
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The Gut-Brain Axis in Healthy Females: Lack of Significant Association between Microbial Composition and Diversity with Psychiatric Measures.
OBJECTIVE: This study examined associations between the composition and diversity of the intestinal microbiota and measures of depression, anxiety, eating disorder psychopathology, stress, and personality in a group of healthy adult females. METHODS: Female participants (n = 91) ages 19-50 years with BMI 18.5-25 kg/m2 were recruited from central North Carolina between July 2014 and March 2015. Participants provided a single fecal sample and completed an online psychiatric questionnaire that included five measures: (i) Beck Anxiety Inventory; (ii) Beck Depression Inventory-II; (iii) Eating Disorder Examination-Questionnaire; (iv) Perceived Stress Scale; and (v) Mini International Personality Item Pool. Bacterial composition and diversity were characterized by Illumina sequencing of the 16S rRNA gene, and associations were examined using Kendall's tau-b correlation coefficient, in conjunction with Benjamini and Hochberg's False Discovery Rate procedure. RESULTS: We found no significant associations between microbial markers of gut composition and diversity and scores on psychiatric measures of anxiety, depression, eating-related thoughts and behaviors, stress, or personality in a large cohort of healthy adult females. DISCUSSION: This study was the first specifically to examine associations between the intestinal microbiota and psychiatric measures in healthy females, and based on 16S rRNA taxonomic abundances and diversity measures, our results do not suggest a strong role for the enteric microbe-gut-brain axis in normal variation on responses to psychiatric measures in this population. However, the role of the intestinal microbiota in the pathophysiology of psychiatric illness may be limited to more severe psychopathology.
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Xiaoyao San reverses the pro-breast cancer effect of depression by inhibiting glutamate levels in intestinal flora.
ETHNOPHARMACOLOGICAL RELEVANCE: Xiaoyao San (XYS), a traditional Chinese herbal remedy used to soothe the liver and resolve depression, has long been employed in the treatment of depression and has recently demonstrated promising effects against breast cancer. However, the exact mechanism of its action against depressive breast cancer remains unclear. AIM OF THE STUDY: This study aimed to identify the molecular targets of XYS responsible for reversing depressive breast cancer and to elucidate its underlying mechanisms. MATERIALS AND METHODS: Behavioral and histopathological analyses will be used to validate the efficacy of XYS in ameliorating depressive breast cancer in chronic unpredictable mild stress (CUMS) models. The differentially expressed genes associated with depressive breast cancer were identified by transcriptomic technology, and network pharmacology was used to predict the target genes of XYS. Furthermore, a pseudogerm-free mouse model was established to explore the mechanistic basis of XYS intervention, and intestinal metabolomics was integrated with 16S rDNA gene sequencing to assess microbiota-related pathways. RESULTS: XYS significantly reversed depression-like behaviors and tumor growth-promoting effects in a CUMS model. Taken together, the results of the transcriptomic data and network pharmacology predictions indicate that XYS may alleviate depression-related breast cancer through modulation of the glutamate receptor signaling pathway. Additional metabolomics and 16S rDNA sequencing studies demonstrated that XYS altered glutamate metabolism in depressive breast cancer mice. Furthermore, the elimination of intestinal flora by antibiotics weakened the efficacy of XYS in the treatment of depressive breast cancer. CONCLUSION: These findings suggest that XYS has potential therapeutic value for treating depressive breast cancer through inhibition of glutamate level within gut microbiota.
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Supplementation with soy isoflavones alleviates depression-like behaviour via reshaping the gut microbiota structure.
Soy isoflavones (SI) are known for their beneficial effects in alleviating neurodegenerative diseases, while the mechanism of alleviation of depression-like behaviour by SI remains unclear. In this study, a chronic unpredictable mild stress (CUMS)-induced depression rat model was used to determine the effect of SI in alleviating depression-like behaviour and its possible mechanisms. SI supplements significantly improved the CUMS-induced depression-like behaviour by increasing the monoamine neurotransmitter levels. A specific SI dose significantly modulated the composition of the gut microbiota, which in turn improved the maximum biotransformation ability of SI. Spearman's correlation analysis illustrated that some of the gut microbiota genera were strongly correlated with monoamine neurotransmitters. Moreover, more attention should be paid to gender differences, which may be related to changes in the gut microbiota. These results suggest that SI might affect monoamine neurotransmitters of CUMS rats by reshaping the structure of the gut microbiota, thereby alleviating depression-like behaviour.
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Gastrodia elata polysaccharide alleviates depression via gut microbiota modulation and Keap1-Nrf2/BDNF-TrkB pathway activation.
Oxidative stress plays a key role in the onset and development of depression, involving dysregulation of intestinal flora and abnormal cell signaling pathways. Gastrodia elata polysaccharide (GEP) presents great potential in neuroprotection and antidepressant effects. However, the specific mechanism underlying its neuroprotective effect remains unclear. This study elucidates how GEP alleviates depression in mice induced by chronic unpredictable mild stress (CUMS) and lipopolysaccharide (LPS). This study investigated the effects of GEP on intestinal flora composition and cell signaling pathways. Additionally, the study investigated its effects in an vitro LPS-induced PC12 cell model. Results indicated that GEP pretreatment effectively mitigated CUMS- and LPS-induced depressive behavior in mice. 16S rRNA sequencing results showed that GEP significantly altered gut microbiota composition in the CUMS model, reduced the Firmicutes/Bacteroidota ratio and increased microbial diversity. Western blotting and qRT-PCR revealed the role of GEP in regulating the Keap1-Nrf2/BDNF-TrkB signaling pathway in vivo and in vitro. Our findings provide insights into the potential mechanisms underlying the neuroprotective effects of GEP while establishing a solid foundation for future utilization of GEP.
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Gastrointestinal Microbiota & Symptoms of Depression and Anxiety in Anorexia Nervosa-A Re-Analysis of the MICROBIAN Longitudinal Study.
The microbiota-gut-brain axis may play a role in the pathophysiology of anorexia nervosa (AN). Here, the relationship between the gastrointestinal microbiota and symptoms of depression, anxiety, and eating disorder pathology in patients with AN before (n = 55) and after weight restoration (n = 44) was investigated by reanalyzing the data of the MICROBIAN study. The gastrointestinal microbiota was analyzed using 16S rRNA amplicon sequencing. Symptoms of anxiety disorder, depression, and the severity of the eating disorder were measured by validated questionnaires. All analyses were adjusted for the body mass index (BMI). Several significant findings between psychological parameters and the gastrointestinal microbiota were not evident after controlling for the BMI. No differences in alpha and beta diversity between groups of higher and lower symptom severity levels for depression and anxiety were found. Positive associations between species of Blautia and Ruminococcus and depression symptoms, and between the phylum Firmicutes and anxiety symptoms were observed after rehabilitation, respectively. A positive correlation was found between propionate and acetate levels and the reduction of depression severity during inpatient treatment. Accounting for the weight status when analyzing the relationship between psychological parameters and the gastrointestinal microbiota in patients with underweight is important since the BMI may be the driver for many observed changes.
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Huangjin Shuangshen Jiawei decoction alleviated coronary heart disease comorbid with depression partly through gut microbiota-mediated regulation of the SRSF1-p53-ASPP1 signaling axis.
BACKGROUND: Coronary heart disease comorbid with depression (CHDD) was associated with poor clinical outcomes and was increasingly linked to gut microbiota dysregulation. Huangjin Shuangshen Jiawei decoction (HJSSJW) showed therapeutic potential in CHDD; however, the microbiota-dependent mechanisms underlying its protective effects remained unclear. PURPOSE: This study was designed to evaluate the effects of HJSSJW on the gut microbiota in murine models of CHDD and to elucidate the potential molecular mechanisms underlying its protective effects. METHODS: The protective effects of HJSSJW were evaluated in a murine model of CHDD using cardiac ultrasound, histopathological analysis, behavioral assessments, and immunofluorescence staining. To investigate the role of the gut microbiota, microbiota depletion was achieved through antibiotic (ABX) treatment, and fecal microbiota transplantation (FMT) was performed to assess microbiota-mediated effects. In parallel, three bacterial strains enriched in CHDD patients following HJSSJW treatment-Faecalibacterium prausnitzii, Parabacteroides goldsteinii, and Butyricicoccus pullicaecorum-were identified and selected for further validation. Their protective effects were further evaluated through colonization experiments in ABX-treated CHDD mice. RESULTS: HJSSJW markedly improved cardiac function in CHDD mice, significantly reduced serum myocardial injury markers, decreased cardiomyocyte apoptosis, and alleviated depressive-like behaviors. In ABX-treated CHDD mice, gut microbiota depletion attenuated the therapeutic efficacy of HJSSJW, whereas FMT from HJSSJW-treated donors partially reproduced these protective effects, suggesting that its actions were at least partially mediated by the gut microbiota. Moreover, colonization with Faecalibacterium prausnitzii, Parabacteroides goldsteinii, or Butyricicoccus pullicaecorum similarly improved cardiac function, reduced myocardial injury markers, attenuated cardiomyocyte apoptosis, and ameliorated depressive-like behaviors in CHDD mice, supporting the contributory roles of these bacteria in the protective effects of HJSSJW. CONCLUSION: HJSSJW exerted coordinated cardioprotective and antidepressant effects in CHDD, which were at least partially mediated by the gut microbiota and were associated with the restoration of the dysregulated SRSF1-p53-ASPP1 signaling axis in cardiac and brain tissues. These findings suggested that HJSSJW might represent a multitarget therapeutic strategy for CHDD and further supported gut microbiota-targeted interventions as a promising therapeutic approach for CHDD.
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[Modulating gut microbiota improves neurological function and depressive symptoms in rats with post-stroke depression].
OBJECTIVE: To evaluate the effect of modulating gut microbiota for improving brain injury in rats with post-stroke depression. METHODS: Adult SD rats were randomized into normal control, middle cerebral artery occlusion (MCAO), post-stroke depression (PSD), PSD with fecal transplantation, PSD with antibiotics (rifaximin), PSD with probiotics (lactobacilli), and PSD with fluoxetine treatment groups (n=9). Neurological function scores of the rats were determined, and the changes in sugar water preference and immobility time in forced swimming test were observed; plasma levels of trimethylamine N-oxide (TMAO) and hydrogen sulfide (H2S) were detected with ELISA, Occludin, and the expressions of occludin, caudin-5 and IgG proteins Ⅰ the brain tissues were determined using Western blotting. RESULTS: Compared with those in the control group, the rats in MCAO and PSD groups had significantly increased neurological function scores, TMAO level, the ratio of TMAO/H2S, and immobility time in forced swimming test with a lowered level of H2S (P < 0.05). These changes were more obvious in PSD rats, which also exhibited a reduced sugar water preference with increased IgG protein and decreased occluding and caudin-5 expressions in the brain tissue (P < 0.05). TMAO/H2S ratio in PSD rats was positively correlated with neurological function score (R2=0.3235, P=0.0269) and immobility time in swimming (R2=0.6290, P=0.0004) and negatively with sugar water preference (R2=-0.4534, P=0.0059). Treatment with fecal transplantation, antibiotics, probiotics and fluoxetine all significantly reduced neurological function scores, immobility time in forced swimming, TMAO/H2S ratio, and IgG protein expression and increased sugar water preference and brain occludin and caudin-5 expressions of the PSD rats (P < 0.05). CONCLUSION: In PSD rats, TMAO/H2S ratio is correlated with neurological function score, immobility time in forced swimming and sugar water preference, and modulating intestinal flora can improve neurological function and depressive symptoms and improve the integrity of the blood-brain barrier.