Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA209717 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The effect of chronic Rapamycin on the transcriptome of old mouse liver
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Project description:Analysis of the effect of gene expression in the livers of old mice (25 months of age) fed rapamycin short term (6 months) Rapamycin from 19 months of age.
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Project description:The effect of Rapamycin on the transcriptome of old mouse liver
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Project description:We previously identified the mTOR pathway as critical to progenitor cell proliferation in a model of liver injury, we investigated the temporal activation of mTOR signaling in a rat model of hepatic carcinogenesis. The model employed chemical carcinogens and partial hepatectomy to induce progenitor marker-positive HCC. Rats were administered the mTOR inhibitor rapamycin for a three week period and liver harvested one month following cessation of rapamycin treatment. Short-term rapamycin treatment resulted in a significant reduction of focal lesion burden. Microarray analysis was performed to characterize the gene expression signature of persistent focal lesions in the rapamcyin and placebo treated animals. This analysis revealed a persistent effect of short-term mTORC1 inhibition on gene expression that resulted in a genetic signature reminiscent of normal liver.
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Project description:Acetaminophen is a widely used antipyretic and analgesic drug, and its overdose is the leading cause of drug-induced acute liver failure. This study aimed to investigate the effect and mechanism of Lacticaseibacillus casei Shirota (LcS), an extensively used and highly studied probiotic, on acetaminophen-induced acute liver injury. C57BL/6 mice were gavaged with LcS suspension or saline once daily for 7 days before the acute liver injury was induced via intraperitoneal injection of 300 mg/kg acetaminophen. The results showed that LcS significantly decreased acetaminophen-induced liver and ileum injury, as demonstrated by reductions in the increases in aspartate aminotransferase, total bile acids, total bilirubin, indirect bilirubin and hepatic cell necrosis. Moreover, LcS alleviated the acetaminophen-induced intestinal mucosal permeability, elevation in serum IL-1α and lipopolysaccharide, and decreased levels of serum eosinophil chemokine (eotaxin) and hepatic glutathione levels. Furthermore, analysis of the gut microbiota and metabolome showed that LcS reduced the acetaminophen-enriched levels of Cyanobacteria, Oxyphotobacteria, long-chain fatty acids, cholesterol and sugars in the gut. Additionally, the transcriptome and proteomics showed that LcS mitigated the downregulation of metabolism and immune pathways as well as glutathione formation during acetaminophen-induced acute liver injury. This is the first study showing that pretreatment with LcS alleviates acetaminophen-enriched acute liver injury, and it provides a reference for the application of LcS.
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Project description:Gene expression in mouse liver in response to short-term calorie restriction
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Project description:Analysis of the effect of gene expression in the livers of old mice (25 months of age) fed rapamycin short term (6 months) Rapamycin from 19 months of age. Total RNA extracted from livers of 25 month old C57BL6/N male and female mice started on control or 14 ppm rapamycin (Rapa) from 19 months of age on 6 months of treatment. Number of samples total: 42, with 10 samples in Control males, 12 samples in Rapa males, 9 samples in Control Females, and 11 samples in Rapa Females
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