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Genipin inhibits LPS-induced acute systemic inflammation in mice

ABSTRACT: Genipin is a natural blue colorant in food industry. Inflammation is correlated with human disorders, and nuclear factor-κB (NF-κB) is the critical molecule involved in inflammation. In this study, the anti-inflammatory effect of genipin on the lipopolysaccharide (LPS)-induced acute systemic inflammation in mice was evaluated by NF-κB bioluminescence-guided transcriptomic analysis. Transgenic mice carrying the NF-κB-driven luciferase genes were administered intraperitoneally with LPS and various amounts of genipin. Bioluminescent imaging showed that genipin significantly suppressed LPS-induced NF-κB-dependent luminescence in vivo. The suppression of LPS-induced acute inflammation by genipin was further evidenced by the reductions of cytokine levels in sera and organs. Microarray analysis of these organs showed that the transcripts of 79 genes were differentially expressed in both LPS and LPS/genipin groups, and one third of these genes belonged to chemokine ligand, chemokine receptor, and interferon (IFN)-induced protein genes. Moreover, network analysis showed that NF-κB played a critical role in the regulation of genipin-affected gene expression. In conclusion, we newly identified that genipin exhibited anti-inflammatory effects in a model of LPSinduced acute systemic inflammation via downregulation of chemokine ligand, chemokine receptor, and IFN-induced protein productions.

ORGANISM(S): Mus musculus

PROVIDER: GSE35934 | GEO | 2012/02/25

SECONDARY ACCESSION(S): PRJNA152075

REPOSITORIES: GEO

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Genipin inhibits LPS-induced acute systemic inflammation in mice

Project description:Genipin is a natural blue colorant in food industry. Inflammation is correlated with human disorders, and nuclear factor-κB (NF-κB) is the critical molecule involved in inflammation. In this study, the anti-inflammatory effect of genipin on the lipopolysaccharide (LPS)-induced acute systemic inflammation in mice was evaluated by NF-κB bioluminescence-guided transcriptomic analysis. Transgenic mice carrying the NF-κB-driven luciferase genes were administered intraperitoneally with LPS and various amounts of genipin. Bioluminescent imaging showed that genipin significantly suppressed LPS-induced NF-κB-dependent luminescence in vivo. The suppression of LPS-induced acute inflammation by genipin was further evidenced by the reductions of cytokine levels in sera and organs. Microarray analysis of these organs showed that the transcripts of 79 genes were differentially expressed in both LPS and LPS/genipin groups, and one third of these genes belonged to chemokine ligand, chemokine receptor, and interferon (IFN)-induced protein genes. Moreover, network analysis showed that NF-κB played a critical role in the regulation of genipin-affected gene expression. In conclusion, we newly identified that genipin exhibited anti-inflammatory effects in a model of LPSinduced acute systemic inflammation via downregulation of chemokine ligand, chemokine receptor, and IFN-induced protein productions. A total of 25 transgenic mice (female, 6 to 8 weeks old) were randomly divided into five groups of five mice: (1) mock, no treatment; (2) LPS (4 mg/kg), (3) LPS plus genipin (1 mg/kg), (4) LPS plus genipin (10 mg/kg), and (5) LPS plus genipin (100 mg/kg). Mice were challenged intraperitoneally with LPS and then with genipin 10 min later. Four hours later, mice were imaged for the luciferase activity, and subsequently sacrificed for ex vivo imaging, RNA extraction, and immunohistochemical staining.

2012-02-25 | E-GEOD-35934 | biostudies-arrayexpress

Assessment of host responses to ionizing radiation

Project description:The aim of this study was to analyze the host responses to ionizing radiation by nuclear factor-κB (NF-κB) bioluminescence imaging-guided transcriptomic tool. Transgenic mice, carrying the NF-κB-driven luciferase gene, were exposed to a single dose of 8.5 Gy total-body irradiation. In vivo imaging showed that a maximal NF-κB-dependent bioluminescent intensity was observed at 3 h after irradiation and ex vivo imaging showed that liver, intestine, and brain displayed strong NF-κB activations. Microarray analysis of these organs showed that irradiation altered gene expression signatures in an organ-specific manner. Pathway analysis showed that pathways associated with metabolism and immune system were altered primarily in liver and intestine. the upregulation of fatty acid binding protein 4, serum amyloid A2, and serum amyloid A3, which are participated in both inflammation and lipid metabolism, suggesting that irradiation might affect the cross pathways of metabolism and inflammation. Moreover, The upregulation of chemokine (CC-motif) ligand 5, chemokine (CC-motif) ligand 20, and Jagged 1 genes suggested that these genes might contribute to the radiation enteropathy. Male transgenic mice (6 to 8 weeks old) were exposed to a single dose of whole-body X-rays generated at 6 MV (Clinac® 21EX medical linear accelerator, Varian, Palo Alto, CA, USA) and at a dose rate of 4 Gy/min. Mice were imaged at 0 h, 1 h, 3 h, 9 h, 24 h, 48 h, or 72 h, or on 7 d or 14 d after irradiation with 8.5 Gy. RNAs were extracted at 3 h after irradiation.

2012-01-01 | E-GEOD-25208 | biostudies-arrayexpress

Assessment of host responses to ionizing radiation

2012-01-01 | GSE25208 | GEO

Rad21-mediated NF-κB signaling limits hematopoietic stem cell self-renewal in aging and inflammation

Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.

2018-11-28 | PXD011537 | Pride

ATAC-seq of primary mammalian aortic endothelial cells before and after TNFα stimulation

Project description:To identify conserved TNFα-induced changes in chromatin-accessibility in mammals, we performed ATAC-seq in primary vascular endothelial cells (ECs) isolated from the aortas of human (HAEC), mouse (MAEC) and cow (BAEC), before and after TNFα. We overlay our data with multi-species NF-κB binding data and identify multiple modes of NF-κB-chromatin interactions that are conserved during mammalian TNFα response. Our cross-species approach identifies conserved changes in chromatin-accessibility at NF-κB binding sites that are disease-relevant and essential during mammalian acute inflammation.

2020-06-01 | E-MTAB-7878 | biostudies-arrayexpress

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

Exploring the effect and mechanism of roselle drink on the urinary tract infection in clinics and the lipopolysaccharide-induced renal inflammation in mice

Project description:Urinary tract infection (UTI) is a common problem in long-term care facilities. Roselle (Hibiscus sabdariffa Linn.) has been used in fold medicine as an anti-inflammatory agent. In this study, we surveyed the effect of roselle drink on the prevention of UTI in long-term care facilities and analyzed the anti-inflammatory potential of roselle on lipopolysaccharide (LPS)-induced renal inflammation. By survey questionnaires, we found that roselle drink was the most commonly used treatment for the routine care of residents. In addition, taking roselle drink in residents with urinary catheters reduced the incidence of UTI by 36%. Roselle suppressed LPS-induced nuclear factor-κB (NF-κB) activation in cells in a dose-dependent manner, and the maximal inhibition (73.75±4.11%) was observed at 100 μg/ml roselle drink. Roselle also suppressed LPS-induced interleukin-1β (IL-1β) production in mice. Gene expression profile of roselle in kidney showed that roselle downregulated the expression of inflammatory genes, and NF-κB was the main transcription factor involved in the regulation of roselle-regulated gene expression. Immunohistochemical staining further showed that roselle inhibited LPS-induced NF-κB activation and inflammatory cell infiltration in kidney. In conclusion, our findings suggested that roselle drink might be a potent benefit herbal supplement for UTI. Moreover, roselle ameliorated LPS-induced renal inflammation via regulating inflammatory gene expression and NF-κB pathway.

2017-08-21 | GSE73939 | GEO

Moringa isothiocyanate-1 inhibits inflammation via NF-κB pathway in skeletal muscle cells

Project description:This study aims to investigate the effect of Moringa isothiocyanate-1 (MIC-1) derived from seeds of Moringa oleifera Lam in lipopolysaccharide (LPS)-induced muscle inflammation models. MIC-1 decreased nitric oxide production, and reduced the expression of pro-inflammatory markers, in C2C12 myoblasts. The daily oral treatment of MIC-1 (80 mg/kg) for three days significantly reduced the expression of pro-inflammatory markers (TNF-α, Ifn-α, IL-1β, IL-6) in gastrocnemius tissue of mice. Transcriptomic analysis provided insight into the inhibitory effects of MIC-1 on the LPS-induced inflammation, which suggests that MIC-1 acts via inflammation, and immunity pathways in myoblasts and skeletal muscle tissue. MIC-1 inhibited the nuclear accumulation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in the LPS-treated murine, which supports that MIC-1 decreases inflammation and regulates immune responses at a gene expression level in LPS-induced inflammation murine model.

2022-07-28 | GSE209706 | GEO

TLR4-NFkB-phospho-NF-kB signaling in BMDM

Project description:The model was constructed to describe TLR4 induced NF-κB activation in native bone marrow-derived macrophages. It included processes of ligand (lipopolysaccharide) recognition, formation of dimer receptor complex and further signal transduction through TRAF6/TAK1 complex that leads to the activation of IKKα/β kinase, which in turn enables the NF-κB transcription factor phosphorylation and translocation in the cell nucleus, and induction of IkB and WIP1 (as an example of induced protein that promotes NF-κB dephosphorylation 2) gene transcription. Models were based on the current knowledge of TLR signaling framework, protein interactions within the TLR4 pathway, and up-to-date mathematical models describing Toll receptor activation. The major important additions were made to TLR4 signaling description: 1) Receptor dimerization process 2) The existence of a basal nuclear NF-κB level (translocation) 3) NF-κB phosphorylation by IKK complex

2019-03-27 | MODEL1809230001 | BioModels

Noncanonical pathway for regulation of CCL2 expression by an mTORC1-FOXK1 axis promotes recruitment of tumor-associated macrophages

Project description:C-C chemokine ligand 2 (CCL2) plays pivotal roles in tumor formation, progression, and metastasis. Although CCL2 expression has been found to be dependent on the nuclear factor (NF)–κB signaling pathway, the regulation of CCL2 production in tumor cells has remained unclear. Mammalian target of rapamycin complex 1 (mTORC1) is a protein kinase that is activated in various tumor cell types. We have now identified a noncanonical pathway for regulation of CCL2 production that is mediated by mTORC1 but independent of NF-κB. Multiple phosphoproteomics approaches identified the transcription factor forkhead box K1 (FOXK1) as a downstream target of mTORC1, with dephosphorylation of FOXK1 in response to mTORC1 activation resulting in transactivation of the CCL2 gene. Inhibition of the mTORC1-FOXK1 axis attenuated insulin-induced CCL2 production as well as the accumulation of tumor-associated monocytes-macrophages and tumor progression in mice. Our results suggest that FOXK1 directly links mTORC1 signaling and CCL2 expression in a manner independent of NF-κB, and that CCL2 produced by this pathway contributes to tumor progression. Specific inhibition of FOXK1 may thus be a potential therapeutic strategy for cancer.

2017-11-30 | PXD007996 | Pride

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