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Baicalin alleviates lipid accumulation in adipocytes via inducing metabolic reprogramming and targeting Adenosine A1 receptor

ABSTRACT: Baicalin alleviates lipid accumulation in adipocytes via inducing metabolic reprogramming and targeting Adenosine A1 receptor

PROVIDER: PRJNA1201196 | ENA |

REPOSITORIES: ENA

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Baicalin alleviates lipid accumulation in adipocytes via inducing metabolic reprogramming and targeting Adenosine A1 receptor

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

Transcriptome analysis of basal and luminal cells treatment with baicalin

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

Transcriptomic Analysis of the Candida albicans Response to Treatment with Baicalin

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

Elucidation of the mechanism behind the potentiating activity of baicalin against Burkholderia cepacia complex biofilms

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

Adenosine Alleviates Necrotizing Enterocolitis by Enhancing the Immunosuppressive Function of MDSCs in Newborns [tissue]

Project description:Adenosine-induced MDSCs represent an essential immune axis for intestinal homeostasis in newborns.

2022-04-18 | GSE200929 | GEO

Adenosine Alleviates Necrotizing Enterocolitis by Enhancing the Immunosuppressive Function of MDSCs in Newborns [cell]

Project description:Adenosine-induced MDSCs represent an essential immune axis for intestinal homeostasis in newborns.

2022-04-18 | GSE200930 | GEO

Acidithiobacillus sp. A1 strain:A1

Project description:Acidithiobacillus sp. A1 strain:A1 Genome sequencing

| PRJNA1031406 | ENA

Gene expression profile in the heart of wild type and Adenosine Receptor A2a over expressing mice

Project description:Adenosine binds to 4 G protein-coupled receptors located on the cardiomyocyte (A1-R, A2a-R, A2b-R and A3-R) and modulates cardiac function during both ischemia and load-induced stress. While the role of adenosine receptor-subtypes has been well defined in the setting of ischemia-reperfusion, far less is known regarding their roles in protecting the heart during other forms of cardiac stress. We characterized the gene expression profiles of heart from A2a-R over-expressing mice subjected to transverse aortic constriction to study the potential of A2a-R activation to protect from pressure-induced heart failure.

2015-03-22 | GSE45423 | GEO

Fusibacter sp. A1 strain:A1

Project description:Fusibacter sp. A1 strain:A1 Genome sequencing and assembly

| PRJNA482918 | ENA

Fusibacter sp. A1 strain:A1

Project description:Fusibacter sp. A1 strain:A1 Genome sequencing and assembly

| PRJNA632469 | ENA