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

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

PROVIDER: PRJNA862131 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20631920.fastq.gz	Fastqsanger.gz
	SRR20631921.fastq.gz	Fastqsanger.gz
	SRR20631922.fastq.gz	Fastqsanger.gz
	SRR20631923.fastq.gz	Fastqsanger.gz
	SRR20631924.fastq.gz	Fastqsanger.gz

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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

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.

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

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

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MiR-520b inhibits endothelial activation by targeting NF-κB p65

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YAP targets TEAD-NF-κB complex and inhibits ccRCC tumor growth

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NF-κB-direct activation of microRNAs with repressive effects on monocyte-specific genes is critical for osteoclast differentiation

Project description:In this study, analysis of miRNA expression changes in osteoclast differentiation from human primary monocytes revealed the rapid upregulation of two miRNA clusters, miR-212/132 and miR-99b/let-7e/125a. We demonstrate that they negatively target monocyte-specific and immunomodulatory genes like TNFAIP3, IGF1R and IL15. Depletion of these miRNAs inhibits osteoclast differentiation and upregulates their targets. These miRNAs are also upregulated in other inflammatory monocytic differentiation processes. Most importantly, we demonstrate for the first time the direct involvement of Nuclear Factor kappa B (NF-κB) in the regulation of these miRNAs, as well as with their targets, whereby NF-κB p65 binds the promoters of these two miRNA clusters and NF-κB inhibition or depletion results in impaired upregulation of their expression. Human primary CD14+ cells isolated from three different donors, and differentiated into osteoclast with MCSF and RANKL for 21 days. miRNA expression analyzed in paired samples at day 0, 2 and 21

2014-12-03 | E-GEOD-63773 | biostudies-arrayexpress

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