Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Polydopamine nanoparticles as a potential pharmaceutical tool in the treatment of non-alcoholic fatty liver disease

ABSTRACT: Non-alcoholic fatty liver disease (NAFLD), or hepatic steatosis, has become one of the most common pathologies among liver-related disorders. The rapid accumulation of fat in this organ, and the consequent increment in oxidative stress levels, have been recognized as one of the main factors involved in the pathological mechanism underlying hepatic steatosis, and progressive non-alcoholic steatohepatitis. Experimental and epidemiological data have shown how antioxidant compounds rich in phenolic groups, such as resveratrol and quercetin, are particular efficient in contrasting the onset of this pathology. In this work, an in vitro model of NAFLD was established based on oleic acid-treated HepG2 cells. Steatotic cells were treated with polydopamine nanoparticles (PDNPs), biocompatible polymeric nanostructures rich in phenolic groups with high antioxidant power. PDNP treatment has shown to be effective in counteracting the hallmarks characterizing hepatic steatosis, and a reduction in the accumulation of lipids has been observed. Further analyses also showed a significant reduction in triglyceride and cholesterol levels, jointly to reduced levels of oxidative stress. Altogether, collected findings suggest PDNPs to be a promising pharmaceutical candidate for the prevention and treatment of hepatic steatosis.

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Liver, Cell Culture

SUBMITTER: Martina Bartolucci

LAB HEAD: Andrea Petretto

PROVIDER: PXD046524 | Pride | 2024-10-02

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20231031_093955_Steatosi.sne	Other
	44SPD_Steatosi_2_A_6.raw	Raw
	44SPD_Steatosi_2_C_8.raw	Raw
	44SPD_Steatosi_2_D_9.raw	Raw
	44SPD_Steatosi_2_E_10.raw	Raw

Items per page:

1 - 5 of 28

Similar Datasets

Hepatocyte Deletion of Triglyceride-Synthesis Enzyme DGAT2 Reduces Steatosis without Increasing Inflammation or Fibrosis

Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by excess lipid accumulation in hepatocytes and reprepresents a huge public health problem owing to its propensity to progress to non-alcoholic steatohepatitis (NASH), fibrosis, and liver failure. The lipids stored in hepatic steatosis are primarily triglycerides (TGs) synthesized by two acyl CoA:diacylglycerol acyltransferase (DGAT) enzymes. Either DGAT1 or DGAT2 catalyzes this reaction, and these enzymes have been suggested to differentially utilize exogenous or endogenously synthesized fatty acids, with DGAT2 being linked to storage of fatty acids from de novo lipogenesis, a process that is increased in NAFLD. However, whether DGAT2 is more responsible for lipid accumulation in NAFLD and the progression to fibrosis is currently unknown. Also, it is unresolved whether DGAT2 can be safely inhibited as a therapy for NAFLD. Here we induced NAFLD-like disease in mice by feeding a diet rich in fructose, saturated fat, and cholesterol and found that hepatocyte-specfici Dgat2 deficiency reduced expression of de novo lipogenesis genes and lowered liver TGs by ~70%. Importantly, the reduction of steatosis was not accompanied by increased inflammation or fibrosis, and insulin and glucose metabolism were unchanged. Conclusion: This study suggests that hepatic DGAT2 deficiency successfully reduced diet-induced hepatic steatosis and supports the development of DGAT2 inhibitors as a therapeutic strategy for treating NAFLD and preventing downstream consequences.

2020-05-26 | PXD013423 | Pride

Expression data from human non-alcoholic fatty liver disease stages

Project description:Global gene expression patterns of 2 human steatosis and 9 human non-alcoholic steatohepatitis (NASH) together with their respective control patterns were analyzed to define the non-alcoholic fatty liver disease (NAFLD) progression molecular characteristics and to define NASH early markers from steatosis. Human liver samples of steatosis and non-alcoholic steatohepatitis were selected for RNA extraction and hybridization on Affymetrix microarrays. This dataset is part of the TransQST collection.

2014-11-07 | E-GEOD-63067 | biostudies-arrayexpress

Classifying distinct grades of human non-alcoholic fatty liver disease employing a systems biology approach

Project description:With an estimated prevalence of about 30% in western countries non-alcoholic fatty liver disease (NAFLD) is a major public health issue [PMID: 18956290]. NAFLD is associated with the metabolic syndrome of insulin resistance, obesity, glucose intolerance. Although many studies are pointing to an induction of insulin resistance by NAFLD causality between both phenotypes is not fully clarified. Furthermore, mechanisms leading to strongly differing progression of NAFLD have to be elucidated which range from mild steatosis up to severe steatohepatitis. Steatohepatitis might even result in liver cirrhosis and hepatocellular carcinoma. Additional complexity is introduced into the understanding of the disease by recent studies providing evidence for a direct development of carcinoma from steatosis without the formerly assumed intermediary phase of cirrhosis. Here, we investigate liver samples from patients with varying severities of steatosis in an integrative approach employing transcriptomics, serum biomarker profling, metabolomics data and systems biology models. Total RNA obtained from hepatocytes derived from nine obese patients with distinct grades of steatosis. This dataset is part of the TransQST collection.

2015-11-01 | E-GEOD-46300 | biostudies-arrayexpress

Diethyldithiocarbamate, an anti-abuse drug, alleviates steatohepatitis and fibrosis in rodents

Project description:C57BL/6 mice received methionine/choline deficient (MCD) diet to establish the model of non-alcoholic fatty liver disease (NAFLD) with or without Diethyldithiocarbamate (DDC) treatment. DDC improves hepatic steatosis, ballooning, inflammation and fibrosis in rodent models of NAFLD through modulating lipid metabolism and oxidative stress.

2018-12-26 | GSE113843 | GEO

Liver proteiomic analysis on westeren diet fed mice under oral supplementation of indole-3-acetate

Project description:Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries. There is growing evidence that dysbiosis of the intestinal microbiota and disruption of microbiota-host interactions contribute to the pathology of NAFLD. We previously demonstrated that gut microbiota derived tryptophan metabolite indole-3-acetate (I3A) was decreased in both cecum and liver of high-fat diet-fed mice and attenuated the expression of inflammatory cytokines in macrophages and TNF-a and fatty acid induced inflammatory responses in an aryl-hydrocarbon receptor (AhR) dependent manner in hepatocytes. In this study, we investigated the effect of orally administered I3A in a mouse model of diet induced NAFLD. Western diet (WD)-fed mice given sugar water (SW) with I3A showed dramatically decreased serum ALT, hepatic TG, liver steatosis, hepatocyte ballooning, lobular inflammation, and hepatic production of inflammatory cytokines, compared to WD-fed mice given only SW. Metagenomic analysis show that I3A administration did not significantly modify the intestinal microbiome, suggesting that I3A’s beneficial effects likely reflect the metabolite’s direct actions on the liver. Administration of I3A partially reversed WD induced alterations of liver metabolome and proteome, notably, decreasing expression of several enzymes in hepatic lipogenesis and β- oxidation. Mechanistically, we also show that AMP-activated protein kinase (AMPK) mediates the anti-inflammatory effects of I3A in macrophages. The potency of I3A in alleviating liver steatosis and inflammation clearly demonstrates its potential as a therapeutic modality for preventing the progression of steatosis to NASH.

2024-02-23 | PXD046255 | Pride

Expression data from liver of Cyclocarya paliurus triterpenic acids treated high-fat-diet-induced mice

Project description:Diverse targets and metabolic pathways are involved in NAFLD, which accounts for the difficulties in achieving the predominant therapeutic effects in clinical practice. Lipid accumulation is the ‘first hit’ in the development of NAFLD in liver, the dysregulation of lipid disposal can lead to hepatic steatosis. Oxidative stress is the ‘second hit’ in the pathogenesis of NAFLD. CP triterpenic acid (CPT) had an ameliorative effect on metabolic diseases, such as non-alcoholic hepatic steatosis. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.

2020-01-01 | GSE125045 | GEO

Differential analysis of gene expression in liver tissues of patients with nonalcoholic fatty liver disease and controls.

Project description:Non-alcoholic fatty liver disease (NAFLD) comprises a collection of chronic liver disorders distinguished by the excessive accumulation of lipids within hepatocytes and the presence of steatosis. It covers a range of liver conditions that vary from simple steatosis (non-alcoholic fatty liver, NAFL) to non-alcoholic steatohepatitis (NASH). In this study, hepatic gene expression was compared among 6 patients with NAFL, 4 with NASH, and 6 healthy controls. All of these samples were collected prior to the liver transplantation procedure. Subsequently, differential genes were identified through comparative analysis of sequencing results, and target genes potentially related to the pathogenesis of NAFLD were further investigated. Numerous potential target genes and pathways have been identified in NAFLD, providing potential targets for therapeutic interventions.

2024-05-15 | GSE260666 | GEO

Malonylation of Acetyl-CoA Carboxylase 1 Promotes Hepatic Steatosis and Is Attenuated by Ketogenic Diet in NAFLD

Project description:Protein post-translational modifications (PTMs) participate in important bioactive regulatory processes and therefore can help elucidate the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Here, we investigate the involvement of PTMs in ketogenic diet (KD)-improved fatty liver by multi-omics and reveal a core target of lysine malonylation, acetyl-CoA carboxylase 1 (ACC1). ACC1 protein levels and Lys1523 malonylation are significantly decreased by KD. It is discovered that a malonylation-mimic mutant in ACC1 increases its enzyme activity and stability to promote hepatic steatosis, whereas the malonylation-null mutant upregulates the ubiquitination degradation of ACC1. A customized Lys1523ACC1 malonylation antibody confirms the increased malonylation of ACC1 in the NAFLD samples. Overall, the lysine malonylation of ACC1 is attenuated by KD in NAFLD and plays an important role in promoting hepatic steatosis. Malonylation is critical for ACC1 activity and stability, highlighting the anti-malonylation effect of ACC1 as a potential strategy for treating NAFLD.

2023-07-21 | PXD040481 | Pride

Transcriptional profiling of mouse liver tissue following control, choline and methonine/choline deficient diet intervention

Project description:Choline and methionine/choline deficient diets are widely used to generate severe rodent hepatic steatosis and steatohepatitis in an attempt to reflect stages of human non-alcoholic fatty liver disease (NAFLD). The underlying mechanism of hepatic injury in these models, and how this reflects human disease remains incompletely understood. We used detailed transcriptional analysis to interrogate the molecular mechanisms of this intervention and its similarity to human disease. Adult C57Bl/6J mice were maintained on control, choline deficient (CDD) or methionine/choline deficient (MCDD) diets for 4 weeks. Isolated liver RNA was used for transcriptional profiling by micro array analysis.

2016-06-01 | E-MTAB-3943 | biostudies-arrayexpress

Microarray analysis among non-alcoholic fatty liver, non-alcoholic steatohepatitis, and type 2 diabetes mellitus rats

Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes. There are 12 samples in our study which belonged to 4 groups, and each group contains 3 different samples.

2015-01-23 | E-GEOD-65220 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data