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

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

PROVIDER: PRJNA454221 | ENA |

REPOSITORIES: ENA

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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

Diethyldithiocarbamate, an anti-abuse drug, alleviates steatohepatitis and fibrosis in rodents through modulating lipid metabolism and oxidative stress.

Project description:Background and purposeDiethyldithiocarbamate (DDC) is a major metabolite of disulfiram that is a potential drug for alcoholism treatment. In the present study, we attempted to explore the possible effect of DDC on non-alcoholic fatty liver disease (NAFLD) and related fibrosis in vivo.Experimental approachC57BL/6 mice and Sprague Dawley (SD) rats received a methionine/choline-deficient (MCD) diet to establish the model of NAFLD with or without DDC treatment. The livers and serum were assessed for histological changes and parameters related to lipid metabolism, liver injury, inflammation and fibrosis. Apoptosis and macrophage related markers were assessed by immunohistochemistry (IHC).Key resultsDDC significantly reduced hepatic steatosis in rats with NAFLD, induced by the MCD diet. DDC reduced the oxidative stress and endoplasmic reticulum stress-related parameters in mice with non-alcoholic steatohepatitis, induced by the MCD diet. IHC for Bax and cleaved caspase-3 showed that DDC inhibited the apoptosis of hepatocytes in the liver. DDC significantly reduced ballooning and Mallory-Denk bodies (MDB) in hepatocytes, accompanied by suppression of serum alanine aminotransferase, aspartate aminotransferase and MDB formation-related genes. DDC significantly alleviated hepatic inflammation, accompanied by suppression of inflammation-related genes. DDC suppressed the infiltration of macrophages, particularly inducible NOS-positive pro-inflammatory macrophages. In addition, DDC significantly alleviated liver fibrosis. Microarray analyses showed that DDC strongly affected lipid metabolism and oxidative stress-related processes and pathways.Conclusion and implicationsDDC improves hepatic steatosis, ballooning, inflammation and fibrosis in rodent models of NAFLD through modulating lipid metabolism and oxidative stress.

| S-EPMC6255958 | biostudies-literature

Moble DNA in Drug Abuse

Project description:Moble DNA in Drug Abuse

| PRJNA603846 | ENA

Moble DNA in Drug Abuse

Project description:Moble DNA in Drug Abuse

| PRJNA603847 | ENA

Tropifexor-Mediated Abrogation of Steatohepatitis and Fibrosis Is Associated With Antioxidative Gene Expression Profile in Rodents

Project description:Tropifexor-Mediated Abrogation of Steatohepatitis and Fibrosis Is Associated With Antioxidative Gene Expression Profile in Rodents

| PRJNA531160 | ENA

Tropifexor-Mediated Abrogation of Steatohepatitis and Fibrosis Is Associated With Antioxidative Gene Expression Profile in Rodents

Project description:Farnesoid X receptor (FXR) agonism is emerging as an important potential therapeutic mechanism of action for multiple chronic liver diseases. The bile acid–derived FXR agonist obeticholic acid (OCA; 6-ethyl chenodeoxycholic acid) has shown promise in a phase 2 study in patients with nonalcoholic steatohepatitis (NASH). Here, we report efficacy of a novel, non–bile acid FXR agonist tropifexor (LJN452) in two distinct preclinical models of NASH. The efficacy of tropifexor at <1 mg/kg doses was superior to that of OCA at 25 mg/kg in the liver in both NASH models. In a chemical and dietary model of NASH (STAM model), tropifexor reversed established fibrosis and reduced nonalcoholic fatty liver disease activity score and hepatic triglycerides. In an insulin-resistant, obese NASH model (AMLN), tropifexor markedly reduced steatohepatitis, fibrosis, and profibrogenic gene expression. Transcriptome analysis of livers from AMLN mice revealed 461 differentially expressed genes following tropifexor treatment, which included a combination of signatures associated with reduction of oxidative stress, fibrogenesis, and inflammation. Conclusion: Based on the preclinical validation in animal models, tropifexor is a promising investigational therapy that is currently under phase 2 development for NASH.

2019-08-20 | GSE129389 | GEO

Paraxonase-2 agonist, Vutiglabridin alleviates non-alcoholic steatohepatitis via autophagy activation

Project description:Paraxonase-2 agonist, Vutiglabridin alleviates non-alcoholic steatohepatitis via autophagy activation

| PRJNA922984 | ENA

PRDX1 Cys52Ser Variant Alleviates Nonalcoholic Steatohepatitis by Reducing Inflammation in Mice

Project description:PRDX1 Cys52Ser Variant Alleviates Nonalcoholic Steatohepatitis by Reducing Inflammation in Mice

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Adolescent Drug Abuse, ADHD and Related Disorders

Project description:Adolescent Drug Abuse, ADHD and Related Disorders

| PRJNA498746 | ENA

Adolescent Drug Abuse, ADHD and Related Disorders

Project description:Adolescent Drug Abuse, ADHD and Related Disorders