Project description:Purpose: a transcriptome analysis was used to ascertain whether lipid metabolism disorders were induced by high-fat diet (HFD), and comparisons were made between control, HFD and DfCS-Ib(treatment) groups. Methods: liver mRNA profiles of C57BL/6 mice were generated by deep sequencing using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: HFD could change the expression of some genes and disturb normal metabolisms. However, there were fewer changes for genes of DfCS-Ib group mice. According to the KEGG Pathway Database and GO analysis, genes involving in lipid biosynthesis, degradation, and transportation were changed by HFD. Conclusions: Our study indicated that DfCS-Ib alleviated lipid disorder of HFD-fed mice in liver by normalizing the expressions of related genes.
Project description:We identified the gene Far2, encoding the fatty acyl-coA reductase 2, to be associated with mesangial matrix expansion (MME) in the mouse (PMID: 24009241). In order to verify this association we obtained the C57BL/6N-Far2tm2a(KOMP)Wtsi/2J (JR#018805) strain from The Jackson Laboratory's KOMP2 program and compared this strain to it's control strain (C57BL/6N) for several renal characteristics. At 6 months of age the knockout mice have a significantly better kidney function (measured as glomerular filtration rate) but the MME is at a comparable level. However, as MME increases in the control strain at 12 months of age, MME does not increase in the knockout until 18 months of age. In order to explore changes at the gene expression level, we compared RNA sequence reads from 6-month old kidneys. Our analysis showed a decrease of RNA expression for several tubular damage markers (NGAL, KIM-1) and an increase in several genes in the fatty acid metabolism pathway.
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.
Project description:Purpose: To study the alteration of whole transcriptome of Lewis lung carcinoma (LLC) cells after the decreasing of malignant properties of tumor by treatment of tumor-bearing mice with RNase A. Methods: Whole transcriptome profile of Lewis lung carcinoma before and after RNase A treatment were generated by deep sequencing using SOLiD 5.5. The sequence reads were mapped by Bioscope 1.3 software, differential expression was evaluated by Cufflinks v.2.0.1 package. Results: Difference in expression was found for 966 genes. Conclusions: Our study represents the first detailed analysis of alteration of transcriptome of Lewis lung carcinoma after the decrease of malignant prtoperties of the tumor (proliferation and invasion) by RNase A.