ABSTRACT
Compound prebiotics (CP) have been explored in modulation of intestinal microbiota and remission of inflammatory responses in the acute colitis (AC). Yet, research on the roles of simultaneous prophylactic and therapeutic CP intervention in relation to AC remains lacking. Here, CP were pre-fed to examine preventive effects. CP, CP combined with mesalazine (5-aminosalicylic acid) (CPM), and mesalazine were used to evaluate therapeutic effects on the dextran sulfate sodium (DSS)-induced AC. Results showed that prophylactic CP and therapeutic CPM alleviated AC, evidenced by variations of body weight, colon length, spleen index, disease activity index score, histological score, and intestinal mucosa. Ruminococcus and Bifidobacterium were detected in significant abundance in the prophylactic CP and therapeutic CPM groups, respectively. Phylogenetic ecological network analysis revealed that therapeutic CPM probably had the strongest coupling between microbes in changing intestinal microbiota to influence treatment. However, changes in short-chain fatty acids (SCFAs) seemed to have no persuasive results, probably due to reduced SCFA level in feces and variability in transit, absorption, and utilization. Furthermore, therapeutic CP exerted higher value in terms of observed species and Shannon diversity, as well as a more concentrated distribution by principal coordinates analysis. Together, the favorable roles of CP in colitis provide directions for prebiotics in designing effective prophylactic functional diets and treatment strategies. KEY POINTS: ⢠Prebiotics as prophylactic intervention effectively inhibited acute colitis. ⢠Prebiotics as prophylactic and therapeutic interventions had distinct effects on gut microbiota. ⢠Prebiotics combined with drug intervention had higher efficacy in treating acute colitis.
Subject(s)
Colitis , Prebiotics , Mice , Animals , Mesalamine/adverse effects , Phylogeny , Colitis/drug therapy , Colitis/prevention & control , Colitis/chemically induced , Colon/microbiology , Disease Models, Animal , Mice, Inbred C57BLABSTRACT
The non-small cell lung cancer (NSCLC) denotes a malignant type of cancers. Long non-coding RNAs (lncRNAs) can actively participate in cancer development. However, the exact role of lncRNAs in NSCLC remains largely elusive. In current work, we report a novel intergenic lncRNA LINC01288 involved in NSCLC. We found that LINC01288 is frequently upregulated in NSCLC samples and cell lines. LINC01288 significantly promotes viability, migration, xenograft tumor growth and metastasis in vitro and in vivo. LINC01288 physically interacts with the IL-6 mRNA and increase the stability of IL-6 transcripts. Subsequently, the autocrine induction of IL-6 and enhanced STAT3 activation may facilitate NSCLC progression. Collectively, our data have demonstrated that LINC01288 serves as a crucial mediator of IL-6/STAT3 pathway and created novel interplay between lncRNAs and tumor development.
Subject(s)
Carcinoma, Non-Small-Cell Lung/genetics , Disease Progression , Interleukin-6/genetics , Lung Neoplasms/genetics , RNA Stability/genetics , RNA, Long Noncoding/genetics , RNA, Messenger/metabolism , Animals , Autocrine Communication , Carcinogenesis/genetics , Carcinoma, Non-Small-Cell Lung/metabolism , Carcinoma, Non-Small-Cell Lung/pathology , Cell Line , Gene Expression Regulation, Neoplastic , Humans , Lung Neoplasms/metabolism , Lung Neoplasms/pathology , Mice , RNA, Messenger/genetics , STAT3 Transcription Factor/metabolism , Xenograft Model Antitumor AssaysABSTRACT
OBJECTIVE: To screen differentially expressed genes of liver tissue in rat sepsis model and analyze them in terms of functions. METHODS: Thirty male Wistar rats were randomly divided into model group and blank control group with 15 rats in each group. Cecal ligation and puncture (CLP) was used to reproduce rat sepsis model, gene expression profile microarray that contains 4 096 rat cDNA clones was used to detect the change in gene expression pattern of rat liver tissue 24 hours after CLP, then differentially expressed genes that high correlated to sepsis were screened, and the functions of these genes were analyzed by means of related computer software. RESULTS: Compared to the controls, gene expression of 522 genes in rat sepsis model were changed 24 hours after CLP, accounting for 12.7%, among them 244 gene expression down-regulated, and 278 gene expression up-regulated. CONCLUSION: Multiple organ dysfunction syndrome (MODS) induced by sepsis involves to a series of gene differential expressions, such as cell cycle and control related genes, cell apoptosis genes, immunity related genes, genes concerning energy metabolism, blood system related genes, cancer related genes, growth factor genes, acute stress reaction related genes etc. Gene microarray technique can be used to comprehensively study gene expression profile in rat sepsis model, in order to find new research objectives and gene therapy strategies for sepsis.