Project description:The objective of this study was to identify the molecular mechanisms and biological pathways associated with the anticancer effects of flaxseed (richest plant source of Omega-3 fatty acid) in laying hen model of ovarian cancer. Study shows a significant reduction in the severity of the disease and increased survival of the laying hens fed with flaxseed.
Project description:Transcriptional profiling of human placenta-derived JEG-3 cell line comparing vehicle control with 7.38 mM of valproic acid(VPA)-treated JEG-3 cells for 48 hr. 7.38 mM valproic acid(VPA) induced the 30% inhibiotion of JEG-3 cell proliferation, G1 phase cell cycle arrest and the reduction of cell size. The Goal was to analyze the mechanism of valproic acid-induced adverse effects in placental cells. Two-condition experiment, JEG-3 cells vs. valproic acid(VPA)-treated JEG-3 cells. Biological replicates: 3 control replicates, 3 VPA-treated replicates.
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
Project description:Interventions: omega-3 fatty acid supplement PO 6.5g/day(including lipid 4g and omega-3 fatty acid 2.2g)
No supplement taking
Primary outcome(s): Reduction of systemic inflammatory response, especially C-reactive protein
Study Design: Parallel Non-randomized
Project description:Despite of the expectation that retinoic acid receptor could be the potential therapeutic targets for pancreatic cancers, there has been the lack of information about the role and the impact of Retinoic acid receptor gamma (RARγ, RARG) on pancreatic cancer, unlike other two RARs.RARG is commonly over-expressed in human pancreatic cancer and is an independent diagnostic marker predicting the poor prognosis of pancreatic cancer patients. In addition, we demonstrated that the reduction in the expression of RARG in human pancreatic cancer cells dramatically suppress their proliferation and tumor growth in vivo, partially attributable to the down-regulation of tumor-supporting biological processes such as glucose transport and the decreased expression of various oncogenes like MYC and STAT3.