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Ursolic acid-induced DECR1 degradation via NF-κB/NLRP3 pathway inihibits vascular calcification

ABSTRACT: Ursolic acid-induced DECR1 degradation via NF-κB/NLRP3 pathway inihibits vascular calcification

PROVIDER: PRJNA1159693 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30630876_1.fastq.gz	Fastqsanger.gz
	SRR30630876_2.fastq.gz	Fastqsanger.gz
	SRR30630877_1.fastq.gz	Fastqsanger.gz
	SRR30630877_2.fastq.gz	Fastqsanger.gz
	SRR30630878_1.fastq.gz	Fastqsanger.gz

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Ursolic acid-induced DECR1 degradation via NF-κB/NLRP3 pathway inihibits vascular calcification

Project description:In this study, we repoort the protective effect of ursolic acid (UA) on vascular calcification in chronic kidney disease. To elucidate the molecular mechanism underlying the anti-vascular calcification effect of UA, we performed RNA-seq to identify the gene expresion under UA treatmment.

2024-09-13 | GSE276910 | GEO

Nanoligomers targeting NF-κB and NLRP3 reduce neuroinflammation and improve cognitive function with aging and tauopathy

Project description:Neuroinflammation contributes to impaired cognitive function in brain aging and neurodegenerative disorders like Alzheimer’s disease, which is characterized by the aggregation of pathological tau. One major driver of both age- and tau-associated neuroinflammation is the NF-κB and NLRP3 signaling axis. However, current treatments targeting NF-κB or NLRP3 may have adverse/systemic effects, and most have not been clinically translatable. Here, we tested the efficacy of a novel, nucleic acid therapeutic (Nanoligomer) cocktail specifically targeting both NF-κB and NLRP3 in the brain for reducing neuroinflammation and improving cognitive function in old wildtype mice, and in a mouse model of tauopathy. We found that 4 weeks of NF-κB/NLRP3-targeting Nanoligomer treatment strongly reduced neuro-inflammatory cytokine profiles in the brain and improved cognitive-behavioral function in both old and tauopathy mice. These effects of NF-κB/NLRP3-targeting Nanoligomer treatment were associated with reduced glial cell activation in old wildtype mice, less pathology in tauopathy mice, favorable changes in transcriptome signatures of inflammation (reduced) and neuronal health (increased) in both mouse models, and no adverse systemic effects. Collectively, our results provide a basis for future translational studies targeting NF-κB/NLRP3 in the brain, perhaps using Nanoligomers, to inhibit neuroinflammation and improve cognitive function with aging and neurodegenerative disease.

2024-02-07 | GSE251888 | GEO

STING facilitates vascular calcification via p-STAT1/NLRP3 signal

Project description:STING facilitates vascular calcification via p-STAT1/NLRP3 signal

| PRJNA1187275 | ENA

Honokiol attenuates oxidative stress and vascular calcification in chronic kidney disease via the upregulation of heme oxygenase-1

Project description:In this study, we repoort the protective effect of ursolic HONOKIOL (HKL) on vascular calcification in chronic kidney disease. To elucidate the molecular mechanism underlying the anti-vascular calcification effect of HKL, we performed RNA-seq to identify the gene expresion under HKL treatmment.

2024-10-12 | GSE278971 | GEO

STING facilitates vascular calcification via p-STAT1/NLRP3 signal

Project description:Vascular calcification contributes to the cardiovascular morbidity and mortality of chronic kidney disease (CKD), but there is no approved treatment for vascular calcification. In this study, we report the role of STING in vascular calcification. To further investigate the molecular mechanism by which STING participates in vascular calcification, we performed high-throughput RNA-seq to identify the target gene of STING.

2024-11-28 | GSE282136 | GEO

S-allylmercaptocysteine Improves NAFLD by Enhancing AhR/Nrf2-mediated Drug Metabolising Enzymes and Reducing NF-κB/IκBα and NLRP3/6-mediated Inflammation

Project description:We investigated the novel molecular mechanisms of the antioxidant and anti-inflammatory properties of S-allylmercaptocysteine (SAMC) based on a transcriptomic study in a non-alcoholic fatty liver disease (NAFLD) rat model. NAFLD was induced in Sprague-Dawley rats by feeding with a high fat diet (HFD) for 12 weeks. 200mg/kg SAMC was fed by oral gavage for 4 weeks from 9-12 week. We found that SAMC co-administration attenuated HFD-induced liver injury, including the increased serum ALT, hepatic oxidative stress and inflammation. Transcriptomic analysis revealed that SAMC dramatically induced the XRE- and ARE-driven drug metabolising enzymes (DMEs) including Akr7a3, Akr1b8, and NQO1. The nuclear translocation of the upstream regulator of xenobiotics metabolism, AhR, and regulator of antioxidant responses, Nrf2, were significantly increased by SAMC treatment. Furthermore, SAMC counteracted the effects of HFD on NF-κB/IκB and NLRP3/6 pathways with decreasing protein levels of ASC, cleaved caspase-1, IL-18 and IL-1β. These results were further verified in another mice NASH model induced by an MCD diet with SAMC co-administration. Conclusion: we propose that SAMC triggers AhR/Nrf2-mediated antioxidant responses which may further suppress the NLRP3/6 inflammasome pathway and NF-κB activation, contributing to the improvement of NAFLD/NASH.

2020-07-20 | GSE150841 | GEO

Downregulation of NF-κB and NLRP3 in aging wildtype and amyloid β transgenic mice

Project description:Neuroinflammation is a key component of Alzheimer's disease (AD), and it may be driven by the activation of NFκB and NLRP3 signaling pathways. AD pathology, like amyloid-β, may exacerbate the activation of these pathways. We used a nucleic acid therapeutic (nanoligomer) cocktail targeting NFκB and NLRP3 to reduce inflamamtory signaling in aged wildtype mice and a transgenic mouse model of amyloid-β pathology (APP/PS1). Short-term (3 days) treatment reversed age- and amyloid-β-related gene sigantures, supporting the idea that this nanoligomer cocktail may have the potential to improve AD-related neuroinflammation and cognitive dysfunction.

2025-07-25 | GSE303458 | GEO

RyR2 inhibitor attenuates cardiac hypertrophy by downregulating TNF-α/NF-κB/NLRP3 signaling pathway

Project description:RyR2 inhibitor attenuates cardiac hypertrophy by downregulating TNF-α/NF-κB/NLRP3 signaling pathway

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Downregulation of NF-κB and NLRP3 in aging wildtype and amyloid β transgenic mice

Project description:Downregulation of NF-κB and NLRP3 in aging wildtype and amyloid β transgenic mice

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RyR2 inhibitor attenuates cardiac hypertrophy by downregulating TNF-α/NF-κB/NLRP3 signaling pathway

Project description:Background: Cardiac Ryanodine receptors (RyR2) can regulate Ca2+ release in the excitation-contraction coupling, when activated, it releases a large amount of Ca2+ into the cytoplasm. Additionally, studies have shown that dantrolene (a RyR2 inhibitor) protects against heart failure and arrhythmias by inhibiting domain decompression, Ca2+ leakage and diastolic Ca2+ sparking. However, the role and mechanism of dantrolene in cardiac hypertrophy remain unclear. Objective: In this study, we aimed to evaluate the therapeutic effects of dantrolene on pressure overload-induced cardiac hypertrophy in mice models by transverse aortic contraction (TAC) surgery and to explore its potential mechanism. Methods: C57/B6 mice (age: 8 weeks) underwent TAC or sham surgical procedure and were administered oral dantrolene (30 mg/kg) or the solvent drug postoperatively. After 4 weeks of drug treatment, RNA sequencing of mice left ventricle was performed.qRT–PCR validation was performed using SYBR Green assays. Results: We found that dantrolene significantly alleviated TAC-induced cardiac hypertrophy. According to RNA sequencing, 184 down-regulated genes were found after dantrolene treatment compared with TAC group, 8 of these were validated with qRT–PCR. According to the KEGG analysis, Creb3l3, IL18R1 and Ccl5 were down-regulated after dantrolene treatment, which were related to TNF-α pathway. Conclusion: As a RyR2 inhibitor, dantrolene attenuates cardiac hypetrophy through downregulating the TNF-α/NF-κB/NLRP3 signaling pathway.

2023-07-01 | GSE184769 | GEO

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