Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Metabolomics reveals the protective effect of isosteviol sodium against multiple organ injury in septic mice - Liver

ABSTRACT: Sepsis is a severe inflammatory disorder that can lead to multiple organ injury. Isosteviol sodium (STV-Na) is a terpenoid derived from stevioside that exerts anti-inflammatory, antioxidant and anticancer activities. However, the influence of STV-Na on sepsis remains unknown. Here, we assessed the potential effects of STV-Na on sepsis and multiple organ injury induced by lipopolysaccharide (LPS). We found that STV-Na increased the survival rate of mice treat with LPS, significantly improved the functions of the heart, lung, liver, and kidney, and reduced the production of inflammatory cytokines. Moreover, Multiorgan metabolomics analysis demonstrated that glutathione metabolism, purine metabolism, glycerophospholipid metabolism and pantothenate and CoA biosynthesis, were significantly altered by STV-Na. This study provides novel insights into the metabolite changes of multiple organ injury in septic mice, which may help characterize the underlying mechanism and provide an improved understanding of the therapeutic effects of STV-Na on sepsis.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Liver

DISEASE(S): Sepsis

SUBMITTER: Shanping Wang

PROVIDER: ST001500 | MetabolomicsWorkbench | Tue Sep 29 00:00:00 BST 2020

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

Metabolomics reveals the protective effect of isosteviol sodium against multiple organ injury in septic mice - Spleen

Project description:Sepsis is a severe inflammatory disorder that can lead to multiple organ injury. Isosteviol sodium (STV-Na) is a terpenoid derived from stevioside that exerts anti-inflammatory, antioxidant and anticancer activities. However, the influence of STV-Na on sepsis remains unknown. Here, we assessed the potential effects of STV-Na on sepsis and multiple organ injury induced by lipopolysaccharide (LPS). We found that STV-Na increased the survival rate of mice treat with LPS, significantly improved the functions of the heart, lung, liver, and kidney, and reduced the production of inflammatory cytokines. Moreover, Multiorgan metabolomics analysis demonstrated that glutathione metabolism, purine metabolism, glycerophospholipid metabolism and pantothenate and CoA biosynthesis, were significantly altered by STV-Na. This study provides novel insights into the metabolite changes of multiple organ injury in septic mice, which may help characterize the underlying mechanism and provide an improved understanding of the therapeutic effects of STV-Na on sepsis.

2020-09-29 | ST001504 | MetabolomicsWorkbench

Metabolomics reveals the protective effect of isosteviol sodium against multiple organ injury in septic mice - Plasma

2020-09-29 | ST001505 | MetabolomicsWorkbench

Metabolomics reveals the protective effect of isosteviol sodium against multiple organ injury in septic mice - Kidney

2020-09-29 | ST001503 | MetabolomicsWorkbench

Metabolomics reveals the protective effect of isosteviol sodium against multiple organ injury in septic mice - Heart

2020-09-29 | ST001499 | MetabolomicsWorkbench

Metabolomics reveals the protective effect of isosteviol sodium against multiple organ injury in septic mice - Lung

2020-09-29 | ST001502 | MetabolomicsWorkbench

Massive Organ Inflammation in Experimental and in Clinical Meningococcal Septic Shock

Project description:The aims of the present study were to investigate the inflammatory responses in various organs as compared with the systemic circulation in an experimental porcine model of meningococcal sepsis using wild-type N. meningitidis; to study the role of LPS versus non-LPS microbial molecules as triggers of organ inflammation in meningococcal sepsis

2022-03-17 | GSE198668 | GEO

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

LPS Tolerance inhibits cellular respiration and induces global changes in the secretome

Project description:Inflammatory response plays an essential role in the resolution of infections. However, inflammation can be detrimental to the organism and cause irreparable damage, for example during sepsis, when a “cytokine storm” can lead to multiple organ failure and often ends in death. One of the strongest triggers of inflammatory response is bacterial lipopolysaccharide (LPS), acting mostly through Toll-like receptor 4 (TLR4). Prior or prolonged exposure to LPS, however, can induce the state of “endotoxin tolerance” where the macrophages and monocytes do not respond to new endotoxin challenge. The cellular mechanisms regulating this phenomenon remain elusive. Our comprehensive secreted protein analysis comparing LPS-tolerant and -responsive monocyte/macrophage-like cells combined with the extracellular flux analysis reveals the robust switch from the inflammatory to metabolic protein expression as well as points to the involvement of specific proteins that may regulate the change from the responsive to the tolerant state

2021-09-09 | PXD021925 | Pride

Deletion of Sufu in macrophages promotes inflammatory responses

Project description:Sepsis is a potentially life-threatening condition caused by the body's response to a severe infection. However, the pathogenesis of sepsis remains unclear. Here, we found that Suppressor of Fused (Sufu), a classical negative regulator of Hedgehog signaling, is downregulated in patients with sepsis and in murine peritoneal macrophages treated with lipopolysaccharide (LPS). Deletion of Sufu aggravated LPS-induced lung injury and lethality in mice, and augmented LPS induced proinflammatory gene expression in cultured macrophages. By RNA-seq transcriptome profiling, we identified Sufu as a negative regulator of the TLR-triggered inflammatory response.

2023-09-12 | GSE234930 | GEO

The H3K4me3 pattern of mouse renal cortex tissues treated with dexmedetomidine against lipopolysaccharide-induced sepsis

Project description:Dexmedetomidine (DEX) was served to controlling the over-reactive inflammatory effects to protect from the sepsis-induced organ failure via modulating histone methylation. However, the genome-wide changes of histone methylations upon DEX for sepsis treatment were poorly explored. (AKI) mouse model was induced by lipopolysaccharide (LPS), and added DEX (AKI+D) and KDM5A-IN-1 (KDM5A inhibitor) (AKI+K) respectively. ChIP-seq to investigate the H3K4me3 pattern in renal cortex tissues. Each group has two replications.

2020-07-03 | E-MTAB-8133 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data