Project description:LEC rats are considered as interesting model for studying hepatitis and development of hepatocarcinogenesis related to copper accumulation and oxidative stress. LEC rats have a mutation in a gene related to liver copper excretion, the Atp7b gene. As a consequence, this rat strain shows an abnormal copper accumulation in the liver. This is believed to be the origin of the acute hepatitis and the subsequent hepatocellular carcinoma that spontaneously develop in these rats. Here, we present the gene expression profiles of LEC rats at different disease stages. LEC rats were classified as normal 6 weeks old (6w), normal 9 weeks old (9w), slight jaundice and jaundice according to age and disease state. D-penicillamine, a copper chelator agent, blocks both hepatitis and tumor development. D-penicillamine-trated LEC rats were used as control rats for gene expression comparison as they showed neither hepatitis development nor tumor marker expression. Gene expression differences in protein metabolism and tumor marker proteins add to the known oxidative stress and inflammation characterization of the hepatitis process, leading to new insights concerning hepatitis and hepatocarcinogenesis development. Keywords: disease state analysis
Project description:LEC rats are considered as interesting model for studying hepatitis and development of hepatocarcinogenesis related to copper accumulation and oxidative stress. LEC rats have a mutation in a gene related to liver copper excretion, the Atp7b gene. As a consequence, this rat strain shows an abnormal copper accumulation in the liver. This is believed to be the origin of the acute hepatitis and the subsequent hepatocellular carcinoma that spontaneously develop in these rats. Here, we present the gene expression profiles of LEC rats at different disease stages. LEC rats were classified as normal 6 weeks old (6w), normal 9 weeks old (9w), slight jaundice and jaundice according to age and disease state. D-penicillamine, a copper chelator agent, blocks both hepatitis and tumor development. D-penicillamine-trated LEC rats were used as control rats for gene expression comparison as they showed neither hepatitis development nor tumor marker expression. Gene expression differences in protein metabolism and tumor marker proteins add to the known oxidative stress and inflammation characterization of the hepatitis process, leading to new insights concerning hepatitis and hepatocarcinogenesis development. Keywords: disease state analysis 6 weeks old LEC rats, 6 rats per group, were sacrified at different hepatitis stages. Biochemical and histological analyses were performed in order to classify the rats into normal, slight jaundice or jaundice groups. D-penicillamine-treated LEC rats (100 mg/kg/day p.o.) were used as control rats since they behave as normal rats. Microarray analysis was performed on liver samples, one replicate per rat, using dyes swap.
Project description:Male Sprague-Dawley rats were used to establish exhausted-exercise model by motorized rodent treadmill. Yu-Ping-Feng-San at doses of 2.18 g/kg was administrated by gavage before exercise training for 10 consecutive days. Quantitative proteomics was performed for assessing the related mechanism of Yu-Ping-Feng-San.
Project description:To explore the gene expression prolife in the chroniclly hypoxic myocardium, 8 rats were divided randomly into normoxic (n=4) or chroniclly hypoxic (n=4) group, and were exposed to room air (21% O2) or continued hypoxia (10% O2) for 4 weeks. Heart tissues were collected and RNA sequencing was applied to detect the overall gene expression prolife. Genes with adjusted P-value ≤0.01 (corrected by Benjamini-Hochberg) and |log2_ratio|≥0.585 are identified as differentially expressed genes. RNA sequencing identified a total of 2014 gene with statistical significances, among which 1260 genes were significantlly increased and 754 genes were significantlly decreased. The results showed that gene expression profiling was perturbed in chronically hypoxic myocardium.
Project description:Knee osteoarthritis (KOA), as a degenerative multifactorial disease, affects the quality of life and mental health of patients, and also brings a huge socioeconomic burden. Treating synovitis have shown promise as anti-inflammatory therapeutics in mitigating OA symptoms and disease progression. Here, by analysing synovial single-cell sequencing (scRNA-seq) data from KOA, we found that synovial fibroblasts (FLS) in OA synovium showed a distinct pro-inflammatory phenotype. We collected synovial tissue from patients with clinical OA as well as from healthy donors, and histological examination was consistent with findings in scRNA-seq. Inspired by recent cross-tissue fibroblast lineage studies, we identified by sequencing that healthy FLS in synovial tissues share transcriptome-level similarities with dermal fibroblasts (DFb). Subsequently, we revealed the local as well as systemic distribution of intra-articular injected DFbs by constructing/extracting two types of rat fibroblasts (luciferase DFbs as well as GFP DFbs). The results demonstrate that DFbs can be locally retained in the synovium for up to three weeks following targeted engrafting on it. And intra-articular injection does not result in DFbs migration to vital organs or the occurrence of histological changes in these organs. A rat model of KOA was constructed by anterior cruciate ligament transection (ACLT) in order to study the therapeutic effect of DFbs on KOA. After injection, the rats showed improvement in painful gait. In addition, histological as well as imaging results showed reduced synovitis and improvement in articular cartilage. Finally we verified the protective effect of DFbs on cytokine-stimulated chondrocytes in a co-culture system.
Project description:Analysis of LBNF1 rat testes from controls, containing both somatic and all germ cell types and from irradiated rats in which all cells germ cells except type A spermatgogonia are eliminated. Results provide insight into distinguishing germ and somatic cell genes and identification of somatic cell genes that are upregulated after irradiation.