Fecal microorganisms
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ABSTRACT:
PROVIDER: PRJNA683668 | ENA |
REPOSITORIES: ENA
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Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide(Dgaln/lps), APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates Dgaln/lps-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against Dgaln/lps-induced hepatocyte injury.
2023-09-01 | GSE241513 | GEO
Project description:Lactobacillus brevis alleviates DSS-induced colitis by reprograming intestinal microbiota and influencing serum metabolome in murine model
| PRJNA564033 | ENA
Project description:DY131 is a pharmacological agonist of the orphan receptor estrogen-related receptor (ERR) γ which plays a crucial role in regulating energy generation, oxidative metabolism, cell apoptosis, inflammatory responses, etc. However, its role in acute liver injury is unknown. In the study, we evaluated the effect of DY131 on lipopolysaccharide (LPS)-induced liver injury. Transcriptomics analysis revealed that the dysregulated pathways associated with inflammation and metabolism were significantly reversed by DY131 in LPS-treated mice, providing more evidence in favor of the protective effect of DY131 against LPS-induced liver injury.
2020-11-06 | GSE160880 | GEO
Project description:This is a randomized, placebo controlled, multicentric trial to investigate the effect of diet supplementation with green tea extract containing 300mg epigallocatechin gallate (EGCG), the major polyphenol of green tea, on the recurrence of colon adenomas.
| 2107175 | ecrin-mdr-crc
Project description:Alzheimer’s disease (AD) is the most common form of adult-onset dementia with severe intellectual deterioration and is characterised by the accumulation of the amyloid-β (Aβ) peptides and the presence of hyperphosphorylated microtubule- associated protein, tau. (-)-Epigallocatechin-3-gallate (EGCG) – a polyphenolic catechin found in green tea leaves, not only acts as a proteasome inhibitor, it is also involved in neuroprotection.
2013-12-31 | GSE22996 | GEO
Project description:Alzheimer’s disease (AD) is the most common form of adult-onset dementia with severe intellectual deterioration and is characterised by the accumulation of the amyloid-β (Aβ) peptides and the presence of hyperphosphorylated microtubule- associated protein, tau. (-)-Epigallocatechin-3-gallate (EGCG) – a polyphenolic catechin found in green tea leaves, not only acts as a proteasome inhibitor, it is also involved in neuroprotection. A total of 7 RNA samples were analyzed. Cultured murine primary cortical neurons were treated with 1uM EGCG for 24h (n=3) in addition to the vehicle control (n=4).
2013-12-31 | E-GEOD-22996 | biostudies-arrayexpress
Project description:Mi(cro)RNAs are small non-coding RNAs of 18-25 nucleotides in length that modulate gene expression at the post-transcriptional level. These RNAs have been shown to be involved in a several biological processes, human diseases and metabolic disorders. Proanthocyanidins, which are the most abundant polyphenol class in the human diet, have positive heath effects on a variety of metabolic disorders such as inflammation, obesity, diabetes and insulin resistance. The present study aimed to evaluate whether proanthocyanidin-rich natural extracts modulate miRNA expression. Using microarray analysis and Q-PCR, we investigated miRNA expression in HepG2 cells treated with proanthocyanidins. Our results showed that when HepG2 cells were treated with grape seed proanthocyanidin extract (GSPE), cocoa proanthocyanidin extract (CPE) or pure epigallocatechin gallate isolated from green tea (EGCG), fifteen, six and five differentially expressed miRNAs, respectively, were identified out of 904 mRNAs. Specifically, miR-30b* was downregulated by the three treatments, and treatment with GSPE or CPE upregulated miR-1224-3p, miR-197 and miR-532-3p. Therefore, these results provide evidence of the capacity of dietary proanthocyanidins to influence microRNA expression, revealing a new mechanism of action of proanthocyanidins. microRNA profiling of Human hepatocellular liver carcinoma cell line (HepG2) comparing control untreated HepG2 cells with cells treated with grape seed proanthocyanidin extract (100 mg/L, 5h), cacao proanthocyanidin extract (100 mg/L, 5h) or epigallocatechin gallate (50 mg/L, 5h). Two biologival replicates were used for control and treated cells with one replicate per array.
2014-07-01 | E-GEOD-30575 | biostudies-arrayexpress
Project description:Global gene profiling of (-)-Epigallocatechin-3-gallate (EGCG)-induced neuronal death
| PRJNA127835 | ENA
Project description:Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an inflammatory process of the lungs characterized by increased permeability of the alveolar-capillary membrane with subsequent interstitial/alveolar edema and diffuse alveolar damage. ALI/ARDS can be the results of either direct or indirect lung injury, with pneumonia being the most common direct pulmonary insult and sepsis the most common extra-pulmonary cause. In this study, we employed the murine lipopolysaccharide (LPS)-induced direct and indirect lung injury model to explore the pathogenic mechanisms of pulmonary and extra-pulmonary ARDS, using an unbiased, discovery and quantitative proteomic approach. A total of 1,017 proteins were both identified and quantified in bronchoalveolar lavage fluid (BALF) from control, intratracheal LPS (I.T. LPS, 0.1 mg/kg) and intraperitoneal LPS (I.P. LPS, 5 mg/kg) treated mice. The two LPS groups shared 13 up-regulated and 22 down-regulated proteins compared to the control group. Among them, molecules related to bronchial and type II alveolar epithelial cell functions including cell adhesion molecule 1 and surfactant protein B were reduced, whereas lactotransferrin and resistin like alpha involved in lung innate immunity were upregulated in both LPS groups. Proteomic profiling also identified significant differences in BALF proteins between I.T. and I.P. LPS groups. Ingenuity pathway analysis revealed that acute-phase response signaling was activated by both I.T. and I.P. LPS, however, the magnitude of activation is much greater in I.T. LPS group compared to I.P. LPS group. Intriguingly, two canonical signaling pathways, liver X receptor/retinoid X receptor activation and the production of nitric oxide and reactive oxygen species in macrophages, were activated by I.T. LPS but suppressed by I.P. LPS. In addition, CXCL15 (also known as lungkine) was also up-regulated by I.T LPS but down-regulated by I.P. LPS. In conclusion, our quantitative discovery-based proteomic approach identified commonalities as well as significant differences in BALF protein expression profiles in LPS-induced direct and indirect lung injury, and importantly, LPS-induced indirect lung injury results in suppression of select components of lung innate immunity, which could contribute to the so-called “immunoparalysis” in sepsis patients.
2019-07-11 | PXD014070 | Pride
Project description:Epigallocatechin-3-gallate (EGCG), a major active polyphenol of green tea, has been shown to downregulate inflammatory responses in macrophages; however, the underlying mechanism has not been understood. Recently, we identified the 67-kDa laminin receptor (67LR) as a cell-surface EGCG receptor that mediates the anti-cancer action of EGCG at physiologically relevant concentrations (0.1-1 mM). Here we show the molecular basis for the downregulation of TLR4 signal transduction by EGCG at 1 mM in macrophages. Anti-67LR antibody treatment or RNAi-mediated silencing of 67LR resulted in abrogation of the inhibitory action of EGCG on LPS-induced activation of downstream signaling pathways and target gene expressions. Additionally, we found that EGCG reduced the TLR4 expression through 67LR. Interestingly, EGCG induced a rapid upregulation of Tollip protein, a negative regulator of TLR-signaling, and this EGCG action was prevented by 67LR silencing or anti-67LR antibody treatment. RNAi-mediated silencing of Tollip impaired the TLR4 signaling inhibitory activity of EGCG. Taken together, these findings demonstrate that 67LR plays a critical role in mediating anti-inflammatory action of a physiologically relevant EGCG and Tollip expression could be modulated through 67LR. These results provide a new insight into the understanding of negative regulatory mechanisms for TLR4 signaling pathway and consequent inflammatory responses which are implicated in the development and progression of many chronic diseases. We quantified expression profile of 210 inflammatory-relating genes in the 67LR-downregulated cells treated with LPS or/and EGCG by microarray
2010-04-20 | E-GEOD-21320 | biostudies-arrayexpress