Gut microbita of luteolin fed mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1159758 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of effect of luteolin on lipid metabolism at gene expression level. The hypothesis tested in the present study was that luteolin treatment with obesogenic diet suppressed the hepatic lipogenesis pathways. Conversely, in adipose tissue, luteolin stimulated the lipogenesis pathway and it also simultaneously increased the expression of genes controlling lipolysis and TCA cycle. Results provide important information about the effect on diet-induced obesity and its metabolic complications. Total RNA of liver and adipose tissues was obtained from normal diet, high-fat diet and luteolin added high-fat diet-fed mice and mRNA expression-associated with lipid metabolism was measured.
2014-09-01 | E-GEOD-54189 | biostudies-arrayexpress
Project description:Although there are studies on obesity and sarcopenia, our understanding of obesity-mediated sarcopenia is insufficient. Additionally, no studies have investigated the application of luteolin in sarcopenia. We attempted to determine the effect of luteolin on obese sarcopenia in mice with high-fat diet (HFD)-induced obesity. Luteolin exerted suppressive effects on obesity, inflammation, and protein degradation in HFD-fed obese mice. Luteolin inhibited lipid infiltration into the muscle and decreased p38 and JNK activity and mRNA expression of inflammatory factors, such as TNFα, Tlr2, Tlr4, MCP1, and MMP2, in the muscle. Suppression of muscle inflammation by luteolin led to the inhibition of myostatin, FoxO, atrogin, and MuRF expression, which reduced protein degradation and improved muscle function. This is the first study to demonstrate that luteolin exerts a protective effect against obese sarcopenia, as its anti-obesity and anti-inflammatory activities inhibited protein degradation. Therefore, luteolin may be a useful supplement for prevention of obese sarcopenia.
2022-07-27 | GSE209778 | GEO
Project description:Gene expression profiling reveals a potential role of Luteolin in LPS induced depression model LPS depression induced mice were orally treated with luteolin (10 mg/kg body weight) once per day during 8 consecutive days. Microarray gene expression was conducted on mice hippocampal tissues. Two mice brains were used for each expermient . The Microarray gene expression was conducted on hipocampus from LPS depression induced mice model(LPS group), LPS depression induced mice model treated with luteolin(LPS+L group), Normal mice (PBS group) and Normal mice treated with luteolin (PBS+L).
2021-11-24 | GSE181285 | GEO
Project description:The flavonoid luteolin possess a variety of anti-inflammatory properties, but little has known about the detailed mechanisms linked to the anti-metabolic syndrome action of luteolin based on the integration of the transcriptional profile and the phenotype biomarkers. The aim of this study was to investigate the protective role of luteolin on inflammation-mediated metabolic diseases, focusing on its role in modulating toll-like receptor (TLR) signaling pathway triggered up-regulation of pro-inflammatory cytokines. Above all, it provides novel insights into the effect of luteolin on the link among adiposopathy, insulin resistance, hepatic steatosis and fibrosis. C57BL/6J mice were fed a normal, high-fat, and high-fat + 0.005% (w/w) luteolin diet for 16 weeks. In this study, (a) luteolin treatment resulted in an improvement in chronic low-grade inflammation by modulating TLR-signaling pathway resulting in reduced pro-inflammatory cytokines and macrophage accumulation; (b) there is a positive relationship of TLR5, MKK4/7, p38 and JNK-related gene expressions and lipogenesis in luteolin-treated obese mice, which is linked to an attenuation of hepatic lipotoxicity with an increased hepatic anti-oxidant system; (c) luteolin prevented hepatic and adipocyte fibrosis by decreasing ECM accumulation and cathepsin gene expressions; (d) Emr1 and Ccl7 genes, important markers inducing low-grade inflammation, are affected by advancing age as well as body weight, and luteolin treatment normalized those gene expressions; (e) luteolin treatment improved insulin resistance by normalizing pancreatic islet dysfunction, and differentially modulating the plasma GLP-1 and GIP levels. Taken together, luteolin ameliorates the deleterious effects of diet-induced obesity and its comorbidity.
2018-03-06 | GSE111412 | GEO
Project description:Gene expression profiling reveals a potential role of Luteolin in LPS induced depression model LPS depression induced mice were orally treated with luteolin (10 mg/kg body weight) once per day during 8 consecutive days. Microarray gene expression was conducted for isolated mice Neural Stem Cells (NSCs) . Two mice brain were used for each expermient. The Microarray gene expression was conducted on NSCs and hipocampus from LPS depression induced depression mice (LPS group), LPS depression induced depression mice treated with luteolin(LPS+L group), Normal mice (PBS group) and Normal mice treated with luteolin (PBS+L).
2021-11-24 | GSE181522 | GEO
Project description:Gut microbiota dysbiosis characterizes systemic metabolic alteration, yet its causality is debated. To address this issue, we transplanted antibiotic-free conventional wild-type mice with either dysbiotic (“obese”) or eubiotic (“lean”) gut microbiota and fed them either a NC or a 72%HFD. We report that, on NC, obese gut microbiota transplantation reduces hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non-transplanted mice. Of note, this phenotype is blunted in conventional NOD2KO mice. By contrast, lean microbiota transplantation did not affect hepatic gluconeogenesis. In addition, obese microbiota transplantation changed both gut microbiota and microbiome of recipient mice. Interestingly, hepatic gluconeogenesis, PEPCK and G6Pase activity were reduced even once mice transplanted with the obese gut microbiota were fed a 72%HFD, together with reduced fed glycaemia and adiposity compared to non-transplanted mice. Notably, changes in gut microbiota and microbiome induced by the transplantation were still detectable on 72%HFD. Finally, we report that obese gut microbiota transplantation may impact on hepatic metabolism and even prevent HFD-increased hepatic gluconeogenesis. Our findings may provide a new vision of gut microbiota dysbiosis, useful for a better understanding of the aetiology of metabolic diseases. all livers are from NC-fed mice only.
2017-03-16 | GSE81318 | GEO
Project description:Gene expression change in the liver of connexin dominant negative transgenic (Tg) and wild-type (Wt) rats fed methionine-choline deficient diet (MCDD) or MCDD with luteolin for 12 weeks.
2017-12-31 | GSE68010 | GEO
Project description:Gut intraepithelial lymphocytes (IELs) are one of the few immune cell populations in the body that expresses glucagon-like 1 receptors (GLP-1R). To test the potential effects of GLP-1 on the gut microbiota through the gut IEL GLP-1R, we performed 16s rRNA seq on the DNA isolated from the fecal pellet of Lck-Cre; Glp1rfl/fl mice (Glp1rTcell-/-) or controls (Glp1rTcell+/+) fed a high-fat diet (HFD) for 12 weeks followed by 1 week of HFD plus semaglutide (10 ug/kg) or vehicle treatment. Fecal pellets from a group of age-matched, sex-matched control mice were included as a chow control group.
2022-08-29 | GSE202452 | GEO
Project description:We observed that luteolin effectively restrained the growth of solid tumors in the established mouse model of HCC. Expression spectrum chip sequencing showed that treatment with luteolin could promote T cell activation, cell chemotaxis and cytokine production. Furthermore, we explored the influence of luteoin on the phenotypic and functional alterations of T cells. Our findings revealed that luteolin maintained a high ratio of CD8+ T cells in the peripheral blood, spleen, and tumor tissues. Additionally, luteolin restored the cytotoxicity of tumor-infiltrating CD8+ T cells in H22 tumor-bearing mice. Moreover, CD8+ T cells showed stronger activation phenotypes and more production of IFN-γ, TNFα, and Granzyme B in serum. Furthermore, the co-administration of luteolin and PD-1 mAb resulted in potentiated anti-tumor effects in H22 tumor-bearing mice.These findings indicate that luteolin could exert an anti-tumor immune response by inducing CD8+ T cell infiltration and enhance the anti-tumor effects of PD-1 mAb in HCC treatment in H22 tumor-bearing mice.
2023-09-20 | GSE243341 | GEO