Gene expression changes in liver tissues from alcohol treated PPARa-null mice
Ontology highlight
ABSTRACT: transcriptomic changes in wild typw and PPARa-null mice fed the Lieber-Decarli liquid diet with or without alcohol for up to four months to identify biomarkers for the early stage of alcohol induced liver damage. Mice were sampled after 1, 2 and 4 months treatment. single-color experiment using Agilent Mouse GE 8x60K Microarray Cat.# G4858A-028005
Project description:transcriptomic changes in the early stages of ALD in mice fed the Lieber-Decarli liquid diet with or without alcohol for four months to identify biomarkers for the early stage of alcohol induced liver damage. Mice were sampled after 1, 2 and 4 months treatment. Two-condition experiment, control vs. alcohol treated at specified time point. Sample pooled from six biological replicates in each group. Reverse-fluorescence replicates.
Project description:transcriptomic changes in wild typw and PPARa-null mice fed the Lieber-Decarli liquid diet with or without alcohol for up to four months to identify biomarkers for the early stage of alcohol induced liver damage. Mice were sampled after 1, 2 and 4 months treatment.
Project description:transcriptomic changes in the early stages of ALD in mice fed the Lieber-Decarli liquid diet with or without alcohol for four months to identify biomarkers for the early stage of alcohol induced liver damage. Mice were sampled after 1, 2 and 4 months treatment.
Project description:The mice were fed with Lieber-Decarli alcohol liquid diet and intraperitoneal injection of carbon tetrachloride to induce alcoholic liver fibrosis in mice. The drug group was treated with kinsenoside at the same time to study the protective effect and mechanism of kinsenoside on alcoholic liver injury in mice.
Project description:Alcoholic liver disease, which varies in severity from mild steatosis to cirrhosis and hepatitis, is one of the most prevalent chronic liver diseases worldwide. Excessive alcohol consumption remains the leading cause of ALD and alcohol-related complications and deaths. However, no medications have been developed to treat this disease and its pathogenesis remains elusive. Here, to understand alcohol-induced AhR activation in more detail, transcriptomic data was conducted using livers from mice subjected to either control or Lieber-DeCarli alcohol diets.
Project description:Chronic alcohol ingestion changes the alveolar landscape. We used microarrays to characterize the change in mRNA expression following chronic alcohol ingestion in male Sprague Dawley rates (EtOH 36% of calories) We used microarrays to characterize the change in mRNA expression following chronic alcohol ingestion in male Sprague Dawley rats (EtOH 36% of calories for 6 weeks). Control animals were given an isocaloric substitution for EtOH for 6 weeks. Alveolar type 2 cells were isolated using an immuno-absorption /technique and RNA was extracted by Trizol. Four control animals and three EtOH treated animals were used for this study.
Project description:Fenofibrate is a specific agonist of the nuclear receptor PPARa. To identify the gene expression under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice. We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice. There are 36 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 14 week-old from the same genetic background (C57Bl/6J) treated with Fenofibrate (100 mg/kg/day) or vehicle (aqueous solution of gum Arabic 3%) by daily gavage for 10 days. n= 4 mice for LKO, LWT and WT genotypes treated with vehicle; n=3 for KO mice treated with vehicle; n=5 mice for LWT, LKO and KO genotypes treated with fenofibrate; n=4 WT mice treated with fenofibrate. All mice were sacrified at ZT14.
Project description:Sprague-Dawley rats were placed on an ethanol-containing or pair-fed Lieber and DeCarli diets for 4 wks prior to surgical fracture. Following insertion of a medullary pin, a closed mid-diaphyseal fracture was induced using a Bonnarens and Einhorn fracture device. At 3 days post-fracture, the region of the fracture calluses were harvested from the right hind-limb. RNA was extracted and microarray analysis was conducted against the entire rat genome to study the effects of alcohol-consumption on the fracture healing. The experiments were on four rat subjects, i.e., pair-fed rats with subsequent surgical fracture or no surgical fracture, and alcohol-fed rats with subsequent surgical fracture or no surgical fracture. Each rat subject described above has three replicates so 6 kinds of pairing can be made and each pairing has a dye-swap replicate (thus, a total 12 array experiments). The focus of this study is on the pair-fed fracture subject vs. alcohol-fed fracture subject.
Project description:If the function of the nuclear receptor PPARa is well-known during a prolongated fasting, its hepatic biological function during feeding and refeeding conditions still needs to be investigated. Moreover, in vivo data collected so far on PPARa function during fasting were obtained using the total Ppara KO transgenic mouse model. To identify genes whose expression is under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice under three nutritional challenges. We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice fed ad libitum, fasted for 24 hours and refed. There are 52 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 8 week-old from the same genetic background (C57Bl/6J) fed ad libitum, fasted for 24 hours, fasted for 24 hours and then refed 24 hours more with glucose added in water (200g/l). In fed condition (Fed), n= 3 mice for LKO, LWT genotypes, n= 5 for KO and n= 4 fot WT; in fasting condition (Fas), n=5 for LKO, LWT and WT genotypes and n= 3 for KO; in refeeding condition (Ref), n= 5 for LKO, KO and WT genotypes and n= 4 for LWT. All mice were sacrified at ZT14.
Project description:Alcohol induced fatty liver cause a dangerous health problem and is the major cause of morbidity and mortality worldwide. Garlic (Allium sativum) is documented to possess anti-fatty liver properties. However the exact molecular mechanisms are unknown. The main aim of this experiment is to elucidate the underlying pathways through which garlic ameliorates alcohol induced fatty liver. Dially disulfide and garlic oil were the garlic compounds used in this study. Leiber DeCarli ethanol liquid diet was to induce fatty liver in C57BL/6 mice model. Also the expression impaired by alcohol induced fatty liver is another aim of this study. Leiber-Decarli ethanol diet was used to induce fatty liver in male C57BL/6 mice (n=12). For control, Lieber-DeCarli liquid control diet was fed to mice (n=4). The control mice were pair-fed to the ethanol mice. After adaptation, the ethanol fed mice were divided into three groups viz. alcohol (n=4), dially disulfide [DADS] (n=4) and garlic oil [GO] (n=4). The study started with the administration of DADS (15 mg/kg bw) or GO (50 mg/kg bw) mixed in 0.1 ml olive oil through gavage. For the control and alcohol groups, same amount of olive oil (0.1 ml) was gavaged. The mice were gavaged daily for 4 weeks. The mice were euthanized by CO2 and blood was collected by cardiac puncture. Liver, kidney, spleen, lungs and hearts were collected and their weights recorded. A portion of liver was snap frozen in liquid nitrogen (200 mg) for RNA extraction.