Project description:Curcumin is a potent modulator of the inflammatory transcriptome in microglia We have performed global gene expression analysis of BV-2 microglial cells under the following conditions: untreated, 20 µM Curcumin-treated, 100ng/ml LPS-treated, or 20 µM Curcumin-treated + 100ng/ml LPS-treated
Project description:Curcumin is a potent anti-inflammatory compound capable of preventing chemically induced colitis in mice. We used microarray analysis to detail the global programme of colonic gene expression in BALB/c mice fed standard or 2% curcumin-supplemented diet and treated with control or TNBS (trnitrobenzene-sulfonic acid, 2 mg/mouse) enema. Keywords: Diet and disease effect.
Project description:Liver fibrosis (LF) is characterized by inflammation and fibrosis following liver injury. Curcumin has anti-inflammatory, antioxidant, and cytoprotective properties, with benefits in managing liver diseases. However, the specific mechanisms underlying these effects remain obscure. This work aims to probe into the potential mechanism of curcumin treating LF.We used CCL4 to construct a liver fibrosis model and treated with low, medium, and high concentrations of curcumin. Subsequently, we collected liver tissues and performed RNA sequencing to identify potential targets and associated signaling pathways affected by curcumin treatment. The results showed that curcumin significantly reduced liver damage in mice induced with carbon tetrachloride. RNA sequencing results indicated that Slamf8 was a likely target and the Slamf8 expression was notably decreased in the curcumin group. According to in vivo and vitro results, curcumin inhibited the TNF/NF-κB pathway via Slamf8 modulation, reducing release of pro-inflammatory cytokines (IL-6, IL-17A, MCP-1). Curcumin also suppressed the expression of LF-associated proteins, including α-SMA, COL1A1 and FN. In summary, curcumin exerts potent anti-fibrotic and anti-inflammatory effects by modulating Slamf8 to influence the TNF/NF-κB pathway, thus protecting the liver.
Project description:Visceral Adipose Tissue (VAT) plays a pivotal role in the systemic metabolic complications of Type 2 Diabetes, acting as a primary site for pro-inflammatory cytokine secretion and lipid storage failure. In this study, we utilized a combined neonatal Streptozotocin (nSTZ) and High-Fat Diet (HFD) model to simulate the progression of diabetic adipopathy in C57BL/6 mice. The objective was to characterize the transcriptomic response of VAT to chronic hyperglycemia and lipid overload, and to evaluate the potential of Curcumin (50 mg/kg) as a metabolic and inflammatory modulator. Following 28 days of daily treatment via oral gavage, VAT samples were collected for total RNA sequencing. These data contribute to the understanding of the molecular mechanisms underlying adipose tissue dysfunction in diabetes and highlight the role of Curcumin in modulating the transcriptomic profile landscape to improve metabolic health.
Project description:We have identified Epigallocatechin Gallate (EGCG) as a potent modulator of microglia function. Our aim was to determine whether EGCG affects the transcriptome of microglia and identify genes and gene sets that may underly the effects of EGCG on microglia function.
Project description:Curcumin is a potent anti-inflammatory compound capable of preventing chemically induced colitis in mice. We used microarray analysis to detail the global programme of colonic gene expression in BALB/c mice fed standard or 2% curcumin-supplemented diet and treated with control or TNBS (trnitrobenzene-sulfonic acid, 2 mg/mouse) enema. Keywords: Diet and disease effect. 6-8 week old BALB/c mice were treated with respective diet two days prior to enema administration (day 0) and sacrificed on day 7. Whole colon was dissected from mice and their wild-type littermates and total RNA isolated for microarray analysis using Affymetrix murine MOE430 mouse array set. RNA was pooled from 3 mice in each dietary/treatment group.
Project description:miRNA profiling of curcumin treated Y79 cells with untreated Y79 cells (control). Aim of the study to see whether any oncogenes or tumor suppressor genes are regulated on curcumin treatment in Y79 cells.
Project description:Iron accumulation in microglia has been observed in Alzheimer’s disease and other neurodegenerative disorders and is thought to contribute to disease progression through various mechanisms including neuroinflammation. To study the interaction between iron accumulation and inflammation, we treated human induced pluripotent stem cell-derived microglia (iPSC-MG) with an increasing concentration of iron, in combination with inflammatory stimuli such as interferon gamma and amyloid β, and performed RNA sequencing.