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Fucoidan reduces NETs accumulation and alleviates chemotherapy-induced peripheral neuropathy

ABSTRACT: Fucoidan reduces NETs accumulation and alleviates chemotherapy-induced peripheral neuropathy

PROVIDER: PRJNA1048422 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27051487_1.fastq.gz	Fastqsanger.gz
	SRR27051487_2.fastq.gz	Fastqsanger.gz
	SRR27051492_1.fastq.gz	Fastqsanger.gz
	SRR27051492_2.fastq.gz	Fastqsanger.gz

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Fucoidan reduces NETs accumulation and alleviates chemotherapy-induced peripheral neuropathy

Project description:Chemotherapy-induced peripheral neuropathy (CIPN) is a serious adverse reaction of chemotherapy with limited treatment. Previous research indicates neutrophil extracellular traps (NETs) is a critical pathogenesis of CIPN. LPS/HMGB1 serve as important inducers of NETs. Here, we aim to target inhibiting NETs formation (NETosis) to alleviate CIPN. Clinically we found the content of LPS, HMGB1 and NETs in the plasma of CIPN patients was significantly increased and positively correlated with VAS scores. Fucoidan decreased LPS/HMGB1/NETs content and relieved CIPN in mice. Mechanistically, fucoidan upregulated the scavenger receptor A1 (SR-A1) expression and promoted bone marrow derived macrophage (BMDM) to phagocytize LPS/HMGB1. Fucoidan also facilitated BMDM to engulf NETs via the recognition and localization of SR-A1 and HMGB1. The therapeutic effects of fucoidan were abolished by SR-A1 knockout. RNA-seq analysis showed that fucoidan significantly increased sqstm1 (p62) gene expression. Fucoidan promoted the competitive binding of sqstm1 and Nrf2 to Keap1, increasing Nrf2 nuclear translocation and SR-A1 transcription. Additionally, microbial diversity sequencing analysis (16S) showed that fucoidan increased gut microbiota diversity and abundance, and upregulated the Bacteroides/Firmicutes ratio. In conclusion, fucoidan promotes SR-A1-mediated phagocytosis of LPS/HMGB1/NETs and maintains gut microbial homeostasis, providing a potential therapeutic strategy for CIPN.

2025-04-09 | GSE249275 | GEO

Fecal microbiota transplantation alleviates diabetes peripheral neuropathy

Project description:Fecal microbiota transplantation alleviates diabetes peripheral neuropathy

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Fucoidan alleviates high-fat diet-induced dyslipidemia and atherosclerosis in ApoEshl mice deficient in apolipoprotein E expression

Project description:Fucoidan, a sulfated polysaccharide extracted from brown seaweeds, possesses many biological activities including anti-inflammatory and anti-oxidant activities. We aimed to investigate the protective effects of fucoidan on dyslipidemia and atherosclerosis in apolipoprotein E-deficient mice (ApoEshl mice) and to elucidate its molecular targets in the liver by using a transcriptomic approach. For 12 weeks, ApoEshl mice were fed a high-fat diet (HFD) supplemented with either 1% or 5% fucoidan. Fucoidan supplementation significantly reduced tissue weight (liver and white adipose tissue), blood lipid, total-cholesterol (TC), triglyceride (TG), non-high density lipoprotein-cholesterol (Non-HDL-C), and glucose levels in HFD-fed ApoEshl mice but increased plasma lipoprotein lipase (LPL) activity and HDL-C levels. Fucoidan also reduced hepatic steatosis levels (liver size, TC and TG levels, and lipid peroxidation) and increased white adipose tissue LPL activity. DNA microarray analysis and quantitative reverse transcription-polymerase chain reaction demonstrated differential expression of genes encoding proteins involved in lipid metabolism, energy homeostasis, and insulin sensitivity, by activating Ppara and inactivating Srebf1. Fucoidan supplementation markedly reduced the thickness of the lipid-rich plaque, lipid peroxidation, and foaming macrophage accumulation in the aorta in HFD-fed ApoEshl mice. Thus, fucoidan supplementation appears to have anti-dyslipidemic and anti-atherosclerotic effects by inducing LPL activity and inhibiting the effects of inflammation and oxidative stress in HFD-fed ApoEshl mice.

2015-12-29 | GSE76374 | GEO

Mechanisms of recalcitrant fucoidan breakdown in marine Planctomycetota

Project description:Marine brown algae produce the highly recalcitrant polysaccharide fucoidan, contributing to long-term oceanic carbon storage and climate regulation. Fucoidan is degraded by specialized heterotrophic bacteria, which promote ecosystem function and global carbon turnover using largely uncharacterized mechanisms. Here, we isolate and study two Planctomycetota strains from the microbiome associated with the alga Fucus spiralis, which grow efficiently on chemically diverse fucoidans. One of the strains appears to internalize the polymer, while the other strain degrades it extracellularly. Multi-omic approaches show that fucoidan breakdown is mediated by the expression of divergent polysaccharide utilization loci, and endo-fucanases of family GH168 are strongly upregulated during fucoidan digestion. Enzymatic assays and structural biology studies reveal how GH168 endo-fucanases degrade various fucoidan cores from brown algae, assisted by auxiliary hydrolytic enzymes. Overall, our results provide insights into fucoidan processing mechanisms in macroalgal-associated bacteria.

2024-11-22 | PXD057797 | Pride

Gut microbiota from healthy donors alleviates peripheral neuropathy in patients with diabetes mellitus

Project description:FMT alleviates peripheral neuropathy in patients with diabetes mellitus

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Anti-proliferation activity of fucoidan on MKN45 gastric cancer cells and downregulation of phosphorylated ASK1, a cell-cycle-regulated cyclin-dependent kinase

Project description:Fucoidan is a high-molecular polysaccharide whose main constituent is sulfated fucose. Extensive studies have demonstrated numerous interesting biological activities for fucoidan. We specifically focused on the anti-proliferation activity of fucoidan and examined the underlying mechanism in MKN45 gastric cancer cells. BrdU assay revealed that fucoidan impeded the MKN45 cell cycle by approximately 50%, and clonogenic assay also showed that fucoidan inhibited cell proliferation. Preliminary examinations of fucoidan using LDH assay showed no immediate cytotoxic effects at 24-h exposure. However, longer time courses revealed inhibition of cell growth at 4 days in a dose-dependent manner. Microarray analysis in MKN45 cells treated with fucoidan identified genes that were upregulated and downregulated in response to fucoidan, including MAP3K5, or ASK1 (apoptosis signal-regulating kinase), which was upregulated by 1.38-fold. Western blot confirmed that fucoidan increased ASK1 protein levels, while reducing the levels of phosphorylated ASK1. Reduction of ASK1 by siRNA decreased proliferation of MKN45 cells. Our findings show that fucoidan may suppress cellular proliferation and DNA synthesis in MKN45 cells by suppressing the ASK1-p38 signaling pathway through reduction of phosphorylated ASK1 levels.

2017-02-09 | GSE58774 | GEO

Expression data from adult wild-type and transgenic zebrafish revealed Oligo-Fucoidan Prevents Radiation induced fibrosis and secondary tumors in zebrafish

Project description:Radiotherapy (RT) often causes unwanted side effects such as radiation-induced fibrosis (RIF) and second malignancies (SM). Fucoidan, a sulfated polysaccharide extracted from brown seaweed, has many biological effects including anti-inflammation and anti-tumor. In the present study, we investigated the radioprotective effect of Oligo-Fucoidan (OF) using zebrafish animal model. Using an oligo-fucoidan oral gavage in wild-type and adult transgenic zebrafish, we then used microarrays to detail the global programme of gene expression after fucoidan treatment and identified distinct classes of up- and down-regulated genes during this process.

2020-04-18 | GSE148811 | GEO

Analysis of fucoidan-induced global transcriptional changes in bone marrow-derived dendritic cells (BMDCs) using RNA-Seq technology

Project description:To investigate the fucoidan-induced global alteration of signalling pathways, we prepared bone marrow-derived dendritic cells (BMDCs) and treated them with fucoidan. We then performed gene expression profiling analysis using RNA-seq data from 6 different cells at one time point.

2022-04-21 | GSE200944 | GEO

Estrogen-induced NETs promote aseptic inflammation via NKCC1 [human]

Project description:Although the formation of neutrophil extracellular traps (NETs) is caused by inflammation-related factors, it remains unclear whether endogenous hormones promote NET formation. Here, we investigate NET formation between infection-driven inflammatory endometrium and estrogen-induced hyperplastic endometrium by single-cell multiomics analysis. We identified a unique neutrophil subpopulation (CD24high neutrophil) involved in estrogen-driven NET formation. Estrogen-induced NETs mainly form due to the imbalance of histone caused by estrogen receptors. Inhibition of NETs significantly ameliorated endometrial hyperplasia (EH) in a murine model. Mechanistically, NETs promote cell proliferation by binding to NKCC1 on epithelial cells. Aspirin was screened to inhibit NET formation and alleviated EH in cynomolgus monkey. This study provides a novel nonhormone replacement therapy to treat patients with estrogen abnormalities by targeting NETs.

2025-01-29 | GSE223639 | GEO

The effect of neutrophil extracellular trap (NETs) on BMDMs

Project description:To investigate the altered gene expression levels in BMDMs treated with or without NETs. Each group had a biological repeat (n=3). Results provide insight into the effect of NETs on BMDMs.

2024-11-27 | GSE268729 | GEO

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