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Sub-chronic exposure of hexaconazole may induce metabolic and neuropathic diseases: The evidence from gut microbiota.
The high-frequency detection and long persistence of hexaconazole (Hex) in agricultural products and environment poses potential risk to non-targeted organisms which should pay special attention to. Intestinal flora plays an important role in host health by prevention the occurrence of various diseases. Therefore, in this study, the disturbance of Hex on intestinal function and flora in rats had been studied at environmental related concentrations to evaluate the potential risk of Hex. Our results showed that Hex exposure induced serious oxidative stress and inflammation in intestinal tract. Meanwhile, it notably decreased the tight connectivity in colonic cell leading to the dysfunction of intestinal barrier. Moreover, 16sRNA gene sequencing showed that Hex exposure significantly disturbed the composition and structures of gut microbiota by decrease beneficial bacteria and increase pathogenic bacteria. Further, the metabolites and SCFAs that related to neuropathic and metabolic diseases in colonic contents were also significantly affected by Hex exposure. The pathways of membrane transport, replication and repair, lipid metabolism, and neurodegenerative diseases had been seriously interfered. The obtained results referred that Hex exposure may pose potential risk to metabolic system causing obesity, metabolic syndrome, and cardiovascular as well as nervous system inducing Parkinson's diseases, Alzheimer's diseases, and depression. Our study provided a new sight to study the mechanisms of Hex induced toxicity effects from the aspect of gut microbiota which could help for prevention the risk induced by Hex.
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Alterations of the gut microbiota in borderline personality disorder.
OBJECTIVE: A growing body of research has shown that people with a wide range of psychiatric disorders, including depression, present with alterations of the gut microbiota, although it is unclear if differences may be caused by the action of psychotropic medication. No data exist for patients with borderline personality disorder (BPD), a psychiatric condition that is frequently comorbidly associated with depression. METHODS: Twenty-four unmedicated patients and twenty-one age- and sex-matched healthy controls were recruited. Stool samples were frozen at -80 °C within ten minutes after defecation. The V4 region of bacterial 16S ribosomal RNA (rRNA) gene was sequenced on an Illumina platform. Operational taxonomic units (OTUs) were used for further analysis of community structure, alpha- and beta-diversity. RESULTS: There was no significant difference in alpha- and beta-diversity between patients and controls. However, the Bacteroidetes/Firmicutes-ratio was higher in patients, approaching significance (p = 0.06, r = 0.23). Four species were significantly less abundant in BPD patients, namely Pseudoflavonifractor phocaensis (p = 0.003, r = 0.41), Eubacterium coprostanoligenes (p = 0.01, r = 0.34), Anaerotaenia torta (p = 0.01, r = 0.35), and (statistically somewhat weaker) Parabacteroides chongii (p = 0.046, r = 0.26), which correlated with various psychometric scores. CONCLUSION: Differences in the taxonomic composition may indicate a potential dysbiosis among SCFA-producing bacteria in BPD. Future research is warranted to replicate these findings in independent and larger samples. If confirmed, the results suggest that microbiota-targeted therapies may be a useful adjunct strategy for BPD.
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Exploring the causal pathway from gut microbiota to polycystic ovary syndrome: A network Mendelian randomization study.
Polycystic ovary syndrome (PCOS) is a complicated endocrine and metabolic syndrome with unclear pathogenesis. The gut microbiota sheds light on the etiology and pathophysiology of PCOS. We used Mendelian randomization (MR) studies to systematically evaluate the pathological mechanism gut microbiota causally associated with PCOS risk. A network MR analysis was performed to estimate the causal effects of gut microbiota and risk factors on PCOS, as well as the mediation effect of risk factors linking gut microbiota to PCOS. The investigation of side effects for the important gut microbiota was subsequently broadened to include phenotypes by performing Phenowide-MR analysis for a range of diseases. Genus Sellimonas id.14369 were causally associated with reduced PCOS risk (odds ratio [OR] = 0.69, 95% confidence interval [CI]: 0.58-0.84, P = 1.22 × 10-4) after multiple testing correction. And Sellimonas retained consistent causal effect estimates after a series of sensitivity analyses. In addition, we observed an indirect effect of Sellimonas on PCOS through body mass index (BMI) using network MR (b = -0.05, 95% CI: -0.09 to -0.01), with a mediated proportion of 12.82% of the total effect. Further, Phenowide-MR analyses showed that the protective effects of Sellimonas on type 2 diabetes and depression (for type 2 diabetes: OR = 0.95, 95% CI: 0.90-0.99, P = .0366; for depression: OR = 0.99, 95% CI: 0.98-1.00, P = .0210). We summarized that the causal path between gut microbiota and type 2 diabetes are also jointly mediated by BMI. Sellimonas may be a protective factor of PCOS, which can affect the occurrence of PCOS through BMI, supporting future studies on the importance of addressing obesity and metabolic issues in preventing and managing PCOS.
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Yunpi Rougan Prescription in Treating Constipation-Predominant IBS: Clinical Observation and Gut Microbiota Effects.
BACKGROUND: Constipation-predominant irritable bowel syndrome (IBS-C) is a chronic functional intestinal disease that can significantly reduce patients' quality of life. OBJECTIVE: This study aims to evaluate the clinical effect and mechanism of YunPi RouGan (YPRG) prescription on IBS-C patients with liver-depression and spleen-deficiency syndrome. METHODS: 42 IBS-C patients receiving treatment at Jiangsu Provincial Hospital of Integrated Traditional Chinese and Western Medicine from May 2022 to March 2023 were recruited and randomly assigned to either the treatment or control group, with 21 patients in each group. The patients received either a YPRG prescription or a linalotide capsule for 4 weeks. A series of scales were utilized to evaluate the clinical symptoms, psychological aspects, and quality of life in IBS patients. Meanwhile, fresh fecal samples were collected to analyze the changes in gut microbiota by 16SrDNA sequencing. RESULTS: In terms of clinical treatment, both YPRG prescription and the first-line drug linaclotide have similar effects for IBS-C. However, YPRG prescription has demonstrated significant improvements in several symptoms, such as abdominal distension and belching. Furthermore, it has been shown to upregulate the diversity of gut microbiota and induce changes in the types of dominant microbiota in IBS-C patients. At the phylum level, Firmicutes and Bacteroides increased, while Proteobacteria, actinobacteria, and desulphurobacteria decreased. At the genus level, Bacteroides, Spirillum, Clostridium praxis, Roxella, Para-salmonella, Haemophilus, koala bacillus, Micrococcus rare, Spirillum, and Streptococcus increased significantly. CONCLUSION: The effect of YPRG prescription on improving the clinical symptoms of IBS-C may be attributed to its potential to regulate gut microbiota.
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Nocturnal light exposure aggravates schizophrenia via gut microbiota mediated lipid metabolism: Human and animal multi-omics evidence.
BACKGROUND: Artificial light at night (ALAN) is common in psychiatric inpatient settings, yet evidence suggests it may exacerbate mental disorders. We aimed to examine the effects of ALAN intervention on schizophrenia relapse risk and the mediating roles of gut microbiota and metabolic pathways. METHODS: Schizophrenia patients in hospital rooms randomly received usual ALAN or reduced ALAN by partially covering lights, and swapped after a two-week washout interval. Outcomes were assessed using the Early Signs Scale (ESS) and Montreal Cognitive Assessment (MoCA). Complementary experiments in a dizocilpine-induced schizophrenia mouse model under ALAN exposure evaluated gut microbiota, metabolomic profiles, and behavioral effects following linoleic acid supplementation. RESULTS: Reduced ALAN exposure was associated with lower ESS scores on depression and incipient psychosis, as well as higher scores on MoCA. These benefits were linked to stabilized gut microbiota and linoleic acid metabolism. There were mediation effects by 13(S)-HpODE (linoleic acid metabolite) on associations of ALAN with higher depression and lower MoCA scores. Mice exposed to ALAN showed gut dysbiosis, disrupted linoleic acid metabolism, and schizophrenia-like behaviors, which were partially ameliorated by linoleic acid supplementation. CONCLUSIONS: ALAN exposure may increase the risk of schizophrenia relapse, potentially mediated by gut microbiota and linoleic acid metabolism. Linoleic acid supplementation indicates potential benefits in rodent models, suggesting a potential translational intervention worthy of further investigation.
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The influence of the brain-gut axis in inflammatory bowel disease and possible implications for treatment.
Brain-gut interactions affect psychological wellbeing and symptom reporting in functional gastrointestinal disorders; the presence of anxiety or depression is associated with the development of new-onset gastrointestinal symptoms, and the presence of gastrointestinal symptoms is associated with the development of psychological disorders de novo. In inflammatory bowel diseases (IBD), the reporting of irritable bowel syndrome (IBS)-type symptoms by patients with quiescent disease is common, and is associated with psychological disorders, impaired quality of life, and increased health-care use. In IBD, data from observational studies suggest that psychological disorders might be associated with relapse of disease activity, and that inflammatory activity is associated with the development of new psychological disorders, as has been described for functional gastrointestinal disorders such as IBS and functional dyspepsia. The brain-gut axis provides the physiological link between the CNS and gastrointestinal tract that might facilitate these relationships. In IBS, treatments targeting disordered brain-gut axis activity, including psychological therapies and antidepressants, might lead to improved symptoms and quality of life. However, in IBD, the benefit of these treatments is less certain because of a scarcity of interventional studies. Despite the scarcity of trials, observational data suggest that the effect of disordered brain-gut axis activity in IBD is substantial, and scope remains for further well designed trials of psychological therapies and antidepressants, particularly in the subset of patients who have coexistent psychological disorders, or in those who report IBS-type symptoms. Integrating these treatments into a biopsychosocial model of care has the potential to improve both psychological wellbeing and quality of life in some patients with IBD, reducing health-care use and altering the natural history of disease.
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Ferulic Acid Alleviates Traumatic Brain Injury and Gastrointestinal Disorders by Promoting Ghrelin to Regulate the Microbiota-Brain-Gut Axis Inflammation and Pyroptosis.
Traumatic brain injury (TBI) is a severe condition with a high mortality rate, affecting multiple organs, including the gastrointestinal (GI) tract. Ghrelin is a brain-gut peptide that regulates the microbiota-brain-gut axis, facilitating communication between the GI tract and the central nervous system. This study aimed to investigate the role of ferulic acid (FA) in regulating Ghrelin to improve TBI and GI disorders (GID) induced by controlled cortical impact (CCI). This study used CCI as the in vivo TBI model and scratch-induced injury of primary astrocytes as the in vitro TBI model. The role and mechanism of FA modulation of Ghrelin in ameliorating TBI and GID were explored using multi-omics and network pharmacology analyses. In vivo, results revealed that FA is the main active component of the Guanxin II compound and mimics its function. Significant improvement in GI hypomotility and brain injury was observed in the FA group compared to the CCI group. Concurrently, FA ameliorated intestinal barrier impairment triggered by CCI-induced reduction in the expression of Ghrelin and reduces the inflammatory response. Furthermore, 16S rRNA results indicated that CCI-induced TBI worsened gut microflora imbalance via the brain-gut axis, while gut dysbiosis aggravated brain injury. FA improved the dysbiosis of Bacteroidetes and Odoribacter mainly by targeting the Ghrelin-mediated inflammatory response. RNA-seq and network pharmacology analyses revealed that FA mainly affects inflammation-mediated pyroptosis pathways in the brain-gut axis. Additionally, experimental evidence demonstrated that FA reversed CCI-induced pyroptosis in rats and scratch injury-induced pyroptosis in astrocytes by promoting the binding of Ghrelin to GHSR, which suppressed the TLR4/NF-κB/NLRP3 pathway. Conclusively, FA could alleviate TBI and GID by promoting Ghrelin to regulate the microbiota-brain-gut axis inflammation via the Ghrelin/TLR4/NLRP3 pathway.
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Golden bifid might improve diarrhea-predominant irritable bowel syndrome via microbiota modulation.
OBJECTIVE: Gut microbiota might play a crucial role in the pathogenesis of irritable bowel syndrome (IBS), and probiotics supplement may be an effective treatment option. This study aims to explore the therapeutic effects of Golden bifid on the diarrhea-predominant IBS (IBS-D). METHODS: Twenty-one consecutive IBS-D patients were recruited based on Rome IV criteria. All patients took 2000 mg Golden bifid triple daily for 4 weeks. Gastrointestinal (GI) symptoms, psychological symptoms, small intestine bacterial overgrowth (SIBO) and fecal microbiota characteristics were evaluated in IBS-D patients before and after treatment. RESULTS: After 4-week treatment of Golden bifid, the GI symptoms such as abdominal pain (2.90 ± 1.04 vs. 1.90 ± 1.26, P = 0.002), abdominal distension (2.00 ± 1.34 vs. 1.29 ± 1.31, P = 0.007), diarrhea (3.24 ± 1.37 vs. 1.81 ± 1.21, P = 0.001), defecatory urgency (3.48 ± 1.03 vs. 2.33 ± 1.35, P = 0.000) and incomplete evacuation (2.71 ± 1.15 vs. 1.76 ± 1.26, P = 0.003) were significantly alleviated in IBS-D patients. The Self-Rating Depression Scale (SDS) decreased significantly (46.19 ± 11.36 vs. 43.33 ± 9.65, P = 0.041), and SIBO could be eradicated in 25% (4/16) of IBS-D patients with SIBO. Meanwhile, the abundance of Unclassified Lachnospiraceae and Dorea in genus level and Unclassified Lachnospiraceae, Bacterium Dorea, Bacterium Butyricicoccus and Dorea formicigenerans ATCC 27755 in species level were increased in fecal microbiota (P < 0.05). CONCLUSIONS: Golden bifid could improve most of GI symptoms and depressive symptoms in IBS-D patients and eradicate a small proportion of SIBO in those IBS-D patients with SIBO. What's more, Golden bifid could also modulate the fecal microbiota in IBS-D patients, which implied that the Golden bifid might improve IBS-D via microbiota modulation.
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Gut Microbiota Composition in Mid-Pregnancy Is Associated with Gestational Weight Gain but Not Prepregnancy Body Mass Index.
BACKGROUND: Pregnancy is a time of numerous hormonal, metabolic, and immunological changes for both the mother and the fetus. Furthermore, maternal gut microbiota composition (GMC) is altered during pregnancy. One major factor affecting GMC in pregnant and nonpregnant populations is obesity. The aim was to analyze associations between maternal overweight/obesity, as well as gestational weight gain (GWG) and GMC. Moreover, the modifying effect of depression and anxiety symptom scores on weight and GMC were investigated. METHODS: Study included 46 women from the FinnBrain Birth Cohort study, of which 36 were normal weight, and 11 overweight or obese according to their prepregnancy body mass index (BMI). Stool samples were collected in gestational week 24, and the GMC was sequenced with Illumina MiSeq approach. Hierarchical clustering was executed to illuminate group formation according to the GMC. The population was divided according to Firmicutes and Bacteroidetes dominance. Symptoms of depression, general anxiety, and pregnancy-related anxiety were measured by using standardized questionnaires. RESULTS: Excessive GWG was associated with distinct GMC in mid-pregnancy as measured by hierarchical clustering and grouping according to Firmicutes or Bacteroidetes dominance, with Bacteroidetes being prominent and Firmicutes being less prominent in the GMC among those with increased GWG. Reduced alpha diversity was observed among the Bacteroidetes-dominated subjects. There were no zero-order effects between the abundances of bacterial genera or phyla, alpha or beta diversity, and prepregnancy BMI or GWG. CONCLUSION: Bacteroidetes-dominated GMC in mid-pregnancy is associated with increased GWG and reduced alpha diversity.
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Reactive oxygen species-responsive prodrug nanomicelle-functionalized Lactobacillus rhamnosus probiotics for amplified therapy of ulcerative colitis.
Characterized by elevated reactive oxygen species (ROS) and disrupted gut flora, ulcerative colitis (UC) affects millions of patients worldwide. Probiotic therapy is commonly utilized in clinical practice to modulate intestinal flora and ameliorate colitis symptoms. Nonetheless, oral probiotics encounter challenges such as limited bioactivity, brief retention time, intricate pathological conditions, and singular efficacy. Here we designed plant-derived 18β-glycyrrhetinic acid (18β-GA) prodrug nanomicelles with ROS and inflammation-resolving capabilities, as well as anti-depressant effects, to protect probiotics and amplify their therapeutic effects in alleviating UC and UC-associated depression-like behaviors. Upon oral administration to UC lesion sites, prodrug nanomicelles can be dissociated by excessive ROS and release 18β-GA to attenuate colonic inflammatory responses and oxidative stress, which in turn provided a favorable microenvironment for LGG to repair intestinal barrier integrity and restore the gut microbiota. The synergistic therapeutic effects of STG nanomicelles and LGG alleviated UC-associated depression-like behavior by suppressing the activation of microglia and reducing neuroinflammation. This study introduces a promising strategy for oral nanomedicine with satisfactory therapeutic outcomes for the treatment of inflammatory diseases by integrating naturally derived small-molecule drugs with probiotics.