Elucidation of the mechanism behind the potentiating activity of baicalin against Burkholderia cepacia complex biofilms
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ABSTRACT:
PROVIDER: PRJEB22888 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2155280.fastq.gz | Fastqsanger.gz | |||
| ERR2155281.fastq.gz | Fastqsanger.gz | |||
| ERR2155282.fastq.gz | Fastqsanger.gz | |||
| ERR2155283.fastq.gz | Fastqsanger.gz | |||
| ERR2155274.fastq.gz | Fastqsanger.gz |
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Project description:Burkholderia cenocepacia J2315 biofilms were described to have an increased susceptibility towards tobramycin when baicalin hydrate was added to the treatment. The goal of this transcriptomic analysis is to elucidate the effect of baicalin hydrate on gene expression levels when added to tobramycin treatment. Therefore, biofilms were grown for 24 hours and treated for another 24 hours with either tobramycin (TOB) (1024ug/ml), baicalin hydrate (BH) (250uM) or a combination of both. Also, an untreated control (physiological saline) was included. This experiment was repeated twice, so three biological replicates per treatment were included for RNAsequencing.
2017-12-04 | E-MTAB-6099 | biostudies-arrayexpress
Project description:Reduced antimicrobial susceptibility due to resistance and tolerance has become a serious threat to human health. An approach to overcome this reduced susceptibility is the use of antibiotic adjuvants, also known as potentiators. These are compounds that have little or no antibacterial effect on their own but increase the susceptibility of bacterial cells towards antimicrobial agents. Baicalin hydrate, previously described as a quorum sensing inhibitor, is such a potentiator that increases the susceptibility of Burkholderia cenocepacia J2315 biofilms towards tobramycin. The goal of the present study is to elucidate the molecular mechanisms behind the potentiating activity of baicalin hydrate and related flavonoids. We first determined the effect of multiple flavonoids on susceptibility of B. cenocepacia J2315 towards tobramycin. Increased antibiotic susceptibility was most pronounced in combination with apigenin 7-O-glucoside and baicalin hydrate. For baicalin hydrate, also other B. cepacia complex strains and other antibiotics were tested. The potentiating effect was only observed for aminoglycosides and was both strain- and aminoglycoside-dependent. Subsequently, gene expression was compared between baicalin hydrate treated and untreated cells, in the presence and absence of tobramycin. This revealed that baicalin hydrate affected cellular respiration, resulting in increased reactive oxygen species production in the presence of tobramycin. We subsequently showed that baicalin hydrate has an impact on oxidative stress via several pathways including oxidative phosphorylation, glucarate metabolism and by modulating biosynthesis of putrescine. Furthermore, our data strongly suggest that the influence of baicalin hydrate on oxidative stress is unrelated to quorum sensing. Our data indicate that the potentiating effect of baicalin hydrate is due to modulating the oxidative stress response, which in turn leads to increased tobramycin-mediated killing.
| S-EPMC5749847 | biostudies-literature
Project description:Baicalin is the main flavonoid component extracted from Scutellaria root. It has multiple potent biological activities, including estrogen-like activity. In our study, we investigated the function of baicalin on mammary stem cell proliferation and mammary development. Our results demonstrated that baicalin significantly accelerates mammary gland development at puberty and during pregnancy; In vitro, baicalin significantly promotes colony formation ability of mammary basal epithelial cells in a three-dimensional (3D) culture system; In vivo, baicalin improved mammary regeneration efficiency in mouse xenograft model. But the mechanism was unknown. Therefore, transcriptome analysis of basal and luminal cells treatment with baicalin was performed.
2021-02-05 | GSE166157 | GEO
Project description:In order to investigate differential gene expression at high resolution, here, we have performed RNA sequencing analysis of samples obtained from Candida albicans cells grown in the presence or absence of baicalin. Overall treatment with baicalin resulted in 496 up-regulated and 346 down-regulated genes.
2025-01-02 | GSE249820 | GEO
Project description:Excessive lipid accumulation can lead to obesity, metabolic-associated fatty liver disease, and type 2 diabetes. However, there are currently few drugs that could effectively and safely inhibit the accumulation of intracellular lipid. In this study, we observed that baicalin significantly altered cellular respiration by reducing mitochondrial oxygen consumption while enhancing glycolytic flux, accompanied by increased phosphorylation of AMPK and ACC, suggesting an adaptation to altered energy availability. Baicalin effectively reduced lipid droplet formation and intracellular triglyceride levels in adipocytes, as marked by downregulating genes and proteins associated with lipid storage, including Cd36, Fabp4, and FASN. Transcriptomic analysis identified 2,150 differentially expressed genes in baicalin-treated adipocytes, with significant enrichment in metabolic pathways such as glycolysis, gluconeogenesis, and lipid metabolism. Further analysis revealed that baicalin upregulated glycolytic and fatty acid β-oxidation (FAO) pathways while downregulating pyruvate dehydrogenase, inducing a shift toward glycolysis and FAO for energy production. Molecular docking analysis revealed that adenosine A1 receptor (ADORA1) was the target of baicalin, which inhibited the maturation of sterol regulatory element binding protein 1 (SREBP1) and finally alleviated lipid deposition. These results demonstrate that baicalin induces metabolic reprogramming of adipocytes by inhibiting glucose aerobic metabolism while enhancing anaerobic glycolysis and FAO. Meanwhile, baicalin targets ADORA1, which subsequently influences the processing of SREBP1 and downregulates lipid biosynthesis, positioning baicalin as a potential therapeutic agent against obesity and related metabolic disorders.
2024-12-25 | GSE285116 | GEO
Project description:The bacterial tyrosine (BY) kinase family comprises the major group of bacterial enzymes endowed with tyrosine kinase activity. We have previously shown that the BceF protein from Burkholderia cepacia IST408 belongs to this BY kinase family and is involved in the biosynthesis of the exopolysaccharide cepacian. However, little is known about the extent of regulation in the cell by this kinase protein. In order to examine this, we performed a comparative transcriptome profile between the bceF mutant and the wild-type B. cepacia IST408. As a control, the transcriptome of another exopolysaccharide-deficient mutant, which had a mutation in the bceE gene, was also determined.
2012-12-01 | GSE38183 | GEO
Project description:Purpose The aim of this study was to investigate the effects of baicalin on septic cardiomyopathy and to elucidate the underlying mechanisms involved. Specifically, this study sought to determine the effects of baicalin on septic cardiomyopathy induced by AC16 cells and LPS in C57BL/6J mice and its underlying mechanisms. Methods: Echocardiography, histological staining, immunoblotting, qPCR, ELISA, RNA-seq, network pharmacology and molecular docking were performed. Changes in cardiomyocytes after LPS injection in mice were observed. The targets of baicalein in septic cardiomyopathy were screened using molecular docking and molecular dynamics, and the pathway of baicalein action was further elucidated by using RNA-seq and network pharmacology. Results: LPS stimulation induced apoptosis, an inflammatory response and oxidative stress in cardiomyocytes. In vivo experiments revealed that baicalin treatment attenuated septic myocardial injury, as evidenced by enhanced cardiac functional parameters, preservation of myocardial structure, and reduced inflammatory/apoptotic responses, and RNA-seq analyses revealed that the Pi3k/AKT signaling pathway was activated after the administration of baicalin, which was verified both in vitro and in vivo; this indicated that the protective effects of baicalin were related to the findings in vitro and in vivo, suggesting that the protective effect of baicalin is related to the activation of the PI3K/AKT pathway. Molecular docking studies revealed that baicalin inhibited cardiomyocyte inflammation and cardiomyocyte apoptosis, thereby ameliorating sepsis-induced cardiac injury, which may be related to the PI3K/Akt pathway. Conclusion: Baicalin activates the PI3K/AKT pathway and protects against sepsis-induced cardiac injury by binding with AKT.
2026-03-24 | GSE292359 | GEO
Project description:To determine if differences in the severity of pulmonary infection in cystic fibrosis been seen in late isolates od Pseudomonas aeruginosa and Burkholderia cepacia are associated with differences in the initial repsonse of alveolar macrophages (AM) to these pathogens, we assessed gene expression changes in human AM in response to infection with a laboratoty strain, early and late clinical isolates of P. aeruginosa, and B. cepacia. Keywords: Comparison of gene expression in alveolar macrophages of normal non-smokers and normal smokers.
2008-07-26 | GSE12245 | GEO