Chemical profiling of Jianwei Xiaoshi oral liquid and its potential mechanism of effect on high-calorie diet-induced dyspepsia in immature rats: gut flora, transcriptomics and network pharmacology
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ORGANISM(S): Rattus norvegicus
PROVIDER: GSE245835 | GEO | 2023/12/31
REPOSITORIES: GEO
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Project description:Chemical profiling of Jianwei Xiaoshi oral liquid and its potential mechanism of effect on high-calorie diet-induced dyspepsia in immature rats: gut flora, transcriptomics and network pharmacology
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Project description:Duodenal Mucosal Barrier in Functional Dyspepsia
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Project description:Duodenal Mucosal Barrier in Functional Dyspepsia [mRNA]
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Project description:Duodenal Mucosal Barrier in Functional Dyspepsia [miRNA]
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Project description:Epithelial Barrier and Leaky Gut in Dyspepsia Running title: Epithelial Barrier and Leaky Gut in Dyspepsia Context: Some studies suggest that FD is associated with ex vivo duodenal epithelial micro-inflammation and barrier impairment; the pathogenesis of these findings is unclear. miRNAs reduce expression of epithelial barrier genes and have been postulated to increase epithelial permeability in irritable bowel syndrome. New findings: Compared to controls, there is reduced mRNA expression of several barrier proteins (zona occludin-1), increased expression of several miRNAs (eg, miR-142-3p) that suppress the genes for barrier proteins in FD. However, mucosal eosinophils, intraepithelial lymphocytes, and mast cells, ex- and in vivo permeability (urinary lactulose and mannitol excretion) were not significantly different in FD. Impact: Patients with FD do not have a leaky gut syndrome.
2023-03-01 | GSE169307 | GEO
Project description:Epithelial Barrier and Leaky Gut in Dyspepsia Running title: Epithelial Barrier and Leaky Gut in Dyspepsia Context: Some studies suggest that FD is associated with ex vivo duodenal epithelial micro-inflammation and barrier impairment; the pathogenesis of these findings is unclear. miRNAs reduce expression of epithelial barrier genes and have been postulated to increase epithelial permeability in irritable bowel syndrome. New findings: Compared to controls, there is reduced mRNA expression of several barrier proteins (zona occludin-1), increased expression of several miRNAs (eg, miR-142-3p) that suppress the genes for barrier proteins in FD. However, mucosal eosinophils, intraepithelial lymphocytes, and mast cells, ex- and in vivo permeability (urinary lactulose and mannitol excretion) were not significantly different in FD. Impact: Patients with FD do not have a leaky gut syndrome.
2023-03-01 | GSE169304 | GEO
Project description:Background: Treatment of functional dyspepsia (FD) in children is generally symptomatic and unsatisfactory. Traditional Chinese medicines, such as Shenqu Xiaoshi Oral Liquid (SXOL), have been recommended to alleviate dyspeptic symptoms. However, evidence of their safety and efficacy remains limited to date. AIM: To assess whether 2 weeks of therapy with SXOL was non-inferior to domperidone syrup in children with FD. Methods: In this randomized, double-blind, double-simulated, non-inferiority, multi-center clinical trial, we recruited children (3-14 years) with FD according to the Rome IV criteria from 17 tertiary medical centers across China. Patients were randomly allocated (1:1) to receive SXOL or domperidone syrup for 2 weeks. We compared the participants' clinical scores from both groups based on the severity and frequency of dyspepsia symptoms according to Rome IV criteria (0, 1, 2, and 4 weeks after randomization). The primary endpoint was the total response rate, which was defined as the proportion of patients with a decrease of 30% or more in the FD symptoms clinical score from baseline, at the end of the 2-weeks treatment. A non-inferiority margin of -10% was set. Secondary endpoints and adverse events were assessed. This trial is registered with www.Chictr.org.cn, number ChiCTR1900022654. Results: Between February 2019 and March 2021, a total of 373 patients were assessed for eligibility, and 356 patients were enrolled and randomized. The clinical response rate at week two was similar for SXOL [118 (83.10%) of 142] and domperidone [128 (81.01%) of 158]; difference 2.09; 95% CI -6.74 to 10.71, thereby establishing non-inferiority. The total FD symptom scores were significantly improved in the two groups at 1-, 2-, and 4-weeks follow-up periods (p < 0.005). The decrease in symptom score compared with the baseline were similar between these two groups. Over the total study period, 10 patients experienced at least one treatment-related adverse event [six (3.37%)] in the SXOL group, four [(2.25%) in the domperidone group], although no serious adverse event was noted. Conclusion: Treatment with SXOL effectively improves dyspeptic symptoms and is well tolerated. In addition, it is not inferior to domperidone syrup and leads to sustained improvement in Chinese children with FD.
| S-EPMC8854498 | biostudies-literature
Project description:Functional dyspepsia (FD) is one of the most prevalent chronic functional gastrointestinal disorders. Several distinct pathophysiological mechanisms, including gastro duodenal motor disorders, visceral hypersensitivity, brain-gut interactions, duodenal subtle inflammation, and genetic susceptibility, have been implicated in the pathogenesis of the disease, so far. However, emerging evidence suggests that both quantitative and qualitative disturbances of the gastrointestinal microbiota may also be implicated. In this context, several studies have demonstrated differences of the commensal bacterial community between patients with FD and healthy controls, while others have shown that intestinal dysbiosis might associate with disease's symptoms severity. Elucidating these complex interactions constituting the microbiota and host crosstalk, may eventually lead to the discovery of novel, targeted therapeutic approaches that may be efficacious in treating the multiple aspects of the disorder. In this review, we summarize the data of the latest research with focus on the association between gut microbiota alterations and host regarding the pathogenesis of FD.
| S-EPMC7285034 | biostudies-literature
Project description:BackgroundQing-Kai-Ling (QKL) oral liquid, evolving from a classical Chinese formula known as An-Gong-Niu-Huang pills, is a well-established treatment for pneumonia with its mechanism remaining muddled. Studies have shown that the regulation of both intestinal flora and host-microbiota co-metabolism may contribute to preventing and treating pneumonia. The study aimed to investigate the potential mechanism by which QKL alleviates pneumonia from the perspective of 'microbiota-metabolites-host' interaction.MethodsWe evaluated the therapeutic effects of QKL on lipopolysaccharide (LPS)-induced pneumonia rats. To explore the protective mechanism of QKL treatment, a multi-omics analysis that included 16S rDNA sequencing for disclosing the key intestinal flora, the fecal metabolome to discover the differential metabolites, and whole transcriptome sequencing of lung tissue to obtain the differentially expressed genes was carried out. Then, a Spearman correlation was employed to investigate the association between the intestinal flora, the fecal metabolome and inflammation-related indices.ResultsThe study demonstrated that pneumonia symptoms were significantly attenuated in QKL-treated rats, including decreased TNF-α, NO levels and increased SOD level. Furthermore, QKL was effective in alleviating pneumonia and provided protection equivalent to that of the positive drug dexamethasone. Compared with the Model group, QKL treatment significantly increased the richness and αlpha diversity of intestinal flora, and restored multiple intestinal genera (e.g., Bifidobacterium, Ruminococcus_torques_group, Dorea, Mucispirillum, and Staphylococcus) that were correlated with inflammation-related indices. Interestingly, the intestinal flora demonstrated a strong correlation with several metabolites impacted by QKL. Furthermore, metabolome and transcriptome analyses showed that enrichment of several host-microbiota co-metabolites [arachidonic acid, 8,11,14-eicosatrienoic acid, LysoPC (20:0/0:0), LysoPA (18:0e/0:0), cholic acid, 7-ketodeoxycholic acid and 12-ketodeoxycholic acid] levels and varying lung gene (Pla2g2a, Pla2g5, Alox12e, Cyp4a8, Ccl19, and Ccl21) expression were observed in the QKL group. Moreover, these metabolites and genes were involved in arachidonic acid metabolism and inflammation-related pathways.ConclusionOur findings indicated that QKL could potentially modulate intestinal flora dysbiosis, improve host-microbiota co-metabolism dysregulation and regulate gene expression in the lungs, thereby mitigating LPS-induced pneumonia in rats. The study may provide new ideas for the clinical application and further development of QKL.
| S-EPMC10288885 | biostudies-literature
Project description:Metabolomics studies hold promise for the discovery of pathways linked to disease processes. Cardiovascular disease (CVD) represents the leading cause of death and morbidity worldwide. Here we used a metabolomics approach to generate unbiased small-molecule metabolic profiles in plasma that predict risk for CVD. Three metabolites of the dietary lipid phosphatidylcholine--choline, trimethylamine N-oxide (TMAO) and betaine--were identified and then shown to predict risk for CVD in an independent large clinical cohort. Dietary supplementation of mice with choline, TMAO or betaine promoted upregulation of multiple macrophage scavenger receptors linked to atherosclerosis, and supplementation with choline or TMAO promoted atherosclerosis. Studies using germ-free mice confirmed a critical role for dietary choline and gut flora in TMAO production, augmented macrophage cholesterol accumulation and foam cell formation. Suppression of intestinal microflora in atherosclerosis-prone mice inhibited dietary-choline-enhanced atherosclerosis. Genetic variations controlling expression of flavin monooxygenases, an enzymatic source of TMAO, segregated with atherosclerosis in hyperlipidaemic mice. Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.
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