Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Kinetic redox proteomic analysis reveals distinct lipopolysaccharide effects, limited by a manganese Superoxide Dismutase mimic

ABSTRACT: Overproduction of reactive oxygen species and antioxidant superoxide dismutases (SOD1, SOD2) dysregulation contribute to chronic inflammatory bowel disease (IBD) pathogenesis. A kinetic redox proteomic strategy (OcSILAC) was used to explore the lipopolysaccharide (LPS) effect, together with the role of the Mn1 SOD-mimic, in the intestinal HT29-MD2 cellular model. Cysteine oxidation was the main early event of LPS treatment, attenuated over 6 h, as counteracted by rapid response systems on both protein levels (SOD1, NQO1, ALDH1) and post-translational levels (oxidized peroxiredoxins), and a late preponderant increased SOD2 level. Mn1 exerted a potent antioxidant effect, limiting the LPS-induced oxidation and increasing antioxidant enzyme levels, and a variable anti-inflammatory effect attenuating the level of most of the LPS-regulated proteins. Our results reveal the multifaceted LPS effect in intestinal epithelial cells (IECs) and highlight Mn1 as a potential effective anti-oxidant and anti-inflammatory agent for IBD treatment, and a useful tool to explore the oxidation and inflammation interconnection.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell

DISEASE(S): Crohn's Disease

SUBMITTER: Giovanni Chiappetta

LAB HEAD: Joelle Vinh

PROVIDER: PXD052414 | Pride | 2025-03-04

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	QE180409_0531_c_mtz.raw	Raw
	QE180409_0532_c_mtz.raw	Raw
	QE180409_0533_c_mtz.raw	Raw
	QE180409_0534_c_mtz.raw	Raw
	QE180409_0535_c_mtz.raw	Raw

Items per page:

1 - 5 of 421

Similar Datasets

Tangeretin alleviates LPS-induced acute lung injury by inhibiting ferroptosis of macrophage via Nrf2 pathways

Project description:Sepsis-induced acute lung injury (ALI) is a severe clinical condition with a high mortality rate. Tangeretin, widely found in citrus fruits, has been reported to exert antioxidant and anti-inflammatory properties. However, whether Tangeretin protects against sepsis-induced ALI and the potential mechanisms remain unclear.We established ALI model via intraperitoneally injected with 5 mg/kg lipopolysaccharides (LPS) for 12 h. Tangeretin was applied intraperitoneally 30 min before LPS treatment. The lung tissue samples from both the LPS and LPS + TAN groups were subjected to RNA sequencing analysis, conducted by OE Biotech Co., Ltd. (Shanghai, China). We performed differential gene expression analysis using RNA-seq data between LPS and LPS/Tangeretin group.GSEA analysis between LPS and LPS/Tangeretin group showed that IL6_JAK_STAT3_SIGNALING, INFLAMMATORY_RESPONSE, TNFA_SIGNALING_VIA_NFKB were significantly enriched (Fig.3C-E). These results identified the anti-inflammatory effect of Tangeretin against sepsis-induced ALI.

2024-01-20 | GSE252755 | GEO

Moringa isothiocyanate-1 regulates Nrf2 and NF-κB Pathway in response to LPS-driven sepsis and inflammation

Project description:Moringa Isothiocyanate-1 (MIC-1) purified from moringa (Moringa oleifera Lam) seed extract (MSE) has been previously proved to modulate anti-inflammatory and antioxidant activities. However, the molecular mechanism remains poorly understood, particularly nothing is known about its effect on Lipopolysaccharide (LPS) induced sepsis/inflammation. Hence, we investigated whether MIC-1 can decrease acute inflammation in the LPS-induced acute inflammation/sepsis model in mice. Mice were treated orally with MIC-1 for three days before the intraperitoneal injection of LPS. MIC-1 treatment resulted in a dramatic improvement in the histopathological signs of inflammation in the liver, kidney, spleen, and colon and a significant reduction of the LPS-induced sepsis. Moreover, MIC-1 treatment significantly reduced the expression of inflammatory markers in all these organs. We also performed transcriptome analysis in vitro and in vivo in LPS induced macrophages and liver with/without MIC-1 treatment. Interestingly, there is an upregulation of inflammatory/immune response genes in LPS induced macrophages/liver, and there is downregulation of same set of genes after treating with MIC-1. Our results together indicate that MIC-1 reduces sepsis/inflammation through NF-κB and Nrf2 mediated anti-inflammatory/antioxidant signaling pathways. Research has demonstrated that chronic low-grade tissue inflammation and oxidative stress are essential factors in the development of metabolic disorders. Therefore, MIC-1 could be a new natural therapeutic strategy to treat metabolic syndrome.

2021-04-07 | GSE155738 | GEO

Effect of melatonin during LPS-induced inflammation on RAW 264.7 cells

Project description:Melatonin is a powerful anti-inflammatory agent and antioxidant. To explore specific anti-inflammatory mechanisms, LPS was used to intervene in RAW 264.7 cells to construct an inflammation model. Then, cells were pretreated with melatonin at concentrations of 10-3M to 10-7M, respectively. The above cells were subjected to DRUG-seq sequencing to explore the specific mechanism of melatonin anti-inflammation.

2024-08-08 | GSE269343 | GEO

Deep proteome analysis of mouse brains from wild-type, LPS-induced, and drug-treated mice groups

Project description:We studied the effect of bacterial Lipopolysaccharides on inducing neuroinflammation in mice. In addition, we investigated the effect of novel LAT1-utilizing anti-inflammatory derivatives on reversing this LPS-induced neuroinflammation status. Thus, we performed deep proteome analysis of mouse brains after treatment with vehicle, LPS, and LPS with LAT1-utilizing derivatives. The objective is to follow the different inflammatory biomarkers in the mouse brain and explain the inflammatory process after the LPS treatment with and without the LAT1-utilizing prodrugs.

2022-10-25 | PXD030838 | Pride

Microarray expression data from iSOD2 adapted livers

Project description:Transient mitochondrial stress can promote beneficial physiological responses and longevity, termed "mitohormesis." To interrogate mitohormetic pathways in mammals, we generated mice in which mitochondrial superoxide dismutase 2 (SOD2) can be knocked-down in an inducible and reversible manner (iSOD2-KD). Depleting SOD2 only during embryonic development did not cause post-natal lethality, allowing us to probe adaptive responses to mitochondrial oxidant stress in adult mice. Liver from adapted mice had increased mitochondrial biogenesis and antioxidant gene expression and fewer reactive oxygen species. Gene expression analysis implicated non- canonical activation of the Nrf2 antioxidant and PPAR-PGC-1 mitochondrial signaling pathways in this response. Transient SOD2 knock-down in embryonic fibroblasts from iSOD2-KD mice also resulted in adaptive mitochondrial changes, enhanced antioxidant capacity, and resistance to a subsequent oxidant challenge. We propose that mitohormesis in response to mitochondrial oxidative stress in mice involves sustained basal activation of mitochondrial and antioxidant signaling pathways to establish a heightened antioxidant state. We used microarrays to determine differentially expressed genes in mouse liver after transient SOD2 knock-down during mouse embryogenesis.

2018-07-06 | GSE116676 | GEO

Expression data from Botryococcus terribilis ethanol extract (BTEE)-treated RAW264 cells

Project description:Gene expression profiling reveals anti-inflammatory effects of BTEE on lipopolysaccharide (LPS)-induced murine RAW264 cells We evaluated the pretreatment effect of BTEE on LPS-induced inflammation in RAW264 cells. Pretreatment with BTEE could significantly attenuate nitric oxide (NO) production and LPS-induced release of inflammatory mediators in RAW264 cells.

2023-04-19 | GSE221665 | GEO

Digestion of whey peptide induces bioactivity on glial cells

Project description:Whey derived peptides have shown potential activity improving brain function in pathological condition. However, there is little information about their mechanism of action on glial cells, which have important immune functions in brain. Astrocytes and microglia are essential in inflammatory and oxidative defense that take place in neurodegenerative disease. In this work we evaluate antioxidant and anti-inflammatory bioactivity of whey peptide in glial cells. Peptides were formed during simulated gastrointestinal digestion (Infogest protocol), and low molecular weight (<5kDA) peptides (WPHf) attenuated reactive oxygen species (ROS) production induced by hydrogen peroxide stimulus in both cells in dose-dependent manner. WPHf induced an increase in the antioxidant glutathione (GSH) content and prevented GSH reduction induced by lipopolysaccharides (LPS) stimulus in astrocytes cells in a cell specific form. An increase in cytokine mRNA expression (TNFalpha and IL6) and nitric oxide secretion induced by LPS was attenuated by WPHf pre-treatment in both cells. The inflammatory pathway was dependent on NFkB activation. Bioactive peptide ranking analysis showed positive correlation with hydrophobicity and negative correlation with high molecular weights. The sequence identification revealed 19 peptides cross-referred with bioactive database for others functions in addition to anti-inflammatory and antioxidant. Bioactive peptides were reach in leucine, valine and tyrosine in the C-terminal region and lysine in the N-terminal region. These proteomics data bring important aspects regarding the mechanism of action in glial cells and the structural-activity relationship of whey peptides resistant to digestion.

2024-04-02 | MSV000094457 | MassIVE

Expression data from BBEE-treated SH-SY5Y cell

Project description:Gene expression profiling reveals anti-inflammatory effects of BBEE on lipopolysaccharide (LPS)-induced Human neuronal SH-SY5Y cells We evaluated the pretreatment effect of BBEE on LPS-induced inflammation in SH-SY5Y cells. Pretreatment with BBEE could significantly attenuate nitric oxide (NO) production and LPS-induced release of inflammatory mediators in SH-SY5Ycells.

2024-08-31 | GSE270419 | GEO

Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells

Project description:Superoxide radical anion and other Reactive Oxygen Species are constantly produced during respiration. In mitochondria, the dismutation of the superoxide radical anion is accelerated by the mitochondrial superoxide dismutase 2 (SOD2), an enzyme that has been traditionally associated with antioxidant protection. However, increases in SOD2 expression promote oxidative stress, indicating that there may be a prooxidant role for SOD2. We show that SOD2, which normally binds manganese, can incorporate iron and generate an alternative isoform with peroxidase activity. The switch from manganese to iron allows FeSOD2 to utilize H2O2 to promote oxidative stress. We found that FeSOD2 is formed in cultured cells. FeSOD2 causes mitochondrial dysfunction and higher levels of oxidative stress in cultured cells. We show that formation of FeSOD2 converts an antioxidant defense into a prooxidant peroxidase that leads to cellular changes seen in multiple human diseases.

2017-12-05 | GSE106206 | GEO

Allocryptopine alleviates IBD through modulating gut microbiota and inhibiting Cx3cl1-Cx3cr1 axis/NF-κB/apoptosis in DSS-induced mice

Project description:To explore the anti-inflammatory bowel disease (IBD) ability of allocryptiine based on label-free quantitative proteomics

2022-12-12 | PXD038736 |