Gut Microbiota Dysbiosis, Oxidative Stress, Inflammation, and Epigenetic Alterations in Metabolic Diseases

Antioxidants, Journal Year: 2024, Volume and Issue: 13(8), P. 985 - 985

Published: Aug. 14, 2024

Gut dysbiosis, resulting from an imbalance in the gut microbiome, can induce excessive production of reactive oxygen species (ROS), leading to inflammation, DNA damage, activation immune system, and epigenetic alterations critical genes involved metabolic pathways. dysbiosis-induced inflammation also disrupt barrier integrity increase intestinal permeability, which allows gut-derived toxic products enter liver systemic circulation, further triggering oxidative stress, associated with diseases. However, specific metabolites, such as short-chain fatty acids (SCFAs), lactate, vitamins, modulate stress system through mechanisms, thereby improving function. microbiota diet-induced diseases, obesity, insulin resistance, dyslipidemia, hypertension, transfer next generation, involving mechanisms. In this review, we will introduce key that, along dysbiosis ROS, are engaged developing Finally, discuss potential therapeutic interventions dietary modifications, prebiotics, probiotics, postbiotics, fecal transplantation, may reduce syndrome by altering alterations. summary, review highlights crucial role pathogenesis a particular focus on (including histone methylomics, RNA interference) that prevent or improve

Language: Английский

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The role of gut microbiota in intestinal disease: from an oxidative stress perspective

Frontiers in Microbiology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 14, 2024

Recent studies have indicated that gut microbiota-mediated oxidative stress is significantly associated with intestinal diseases such as colorectal cancer, ulcerative colitis, and Crohn’s disease. The level of reactive oxygen species (ROS) has been reported to increase when the microbiota dysregulated, especially several bacterial metabolites are present. Although healthy plays a vital role in defending against excessive stress, disease influenced by ROS, this process controlled immunological responses, DNA damage, inflammation. In review, we discuss relationship between from an perspective. addition, also provide summary most recent therapeutic approaches for preventing or treating modifying microbiota.

Language: Английский

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The emerging role of oxidative stress in inflammatory bowel disease

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: July 15, 2024

Inflammatory bowel disease (IBD) is a chronic immune-mediated condition that affects the digestive system and includes Crohn’s (CD) ulcerative colitis (UC). Although exact etiology of IBD remains uncertain, dysfunctional immunoregulation gut believed to be main culprit. Amongst immunoregulatory factors, reactive oxygen species (ROS) nitrogen (RNS), components oxidative stress event, are produced at abnormally high levels in IBD. Their destructive effects may contribute disease’s initiation propagation, as they damage lining activate inflammatory signaling pathways, further exacerbating inflammation. Oxidative markers, such malondialdehyde (MDA), 8-hydroxy-2’-deoxyguanosine (8-OHdG), serum-free thiols (R-SH), can measured blood stool patients with These markers elevated IBD, their correlate severity disease. Thus, used not only diagnosis but also monitoring response treatment. It targeted treatment through use antioxidants, including vitamin C, E, glutathione, N-acetylcysteine. In this review, we summarize role pathophysiology its diagnostic targets, potential application antioxidant therapies manage treat

Language: Английский

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Oxidative Stress and Reprogramming of Lipid Metabolism in Cancers

Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 201 - 201

Published: Feb. 10, 2025

Oxidative stress is a common event involved in cancer pathophysiology, frequently accompanied by unique lipid metabolic reprogramming phenomena. caused mainly an imbalance between the production of reactive oxygen species (ROS) and antioxidant system cells. Emerging evidence has reported that oxidative regulates expression activity metabolism-related enzymes, leading to alteration cellular metabolism; this involves significant increase fatty acid synthesis shift way which lipids are taken up utilized. The dysregulation metabolism provides abundant intermediates synthesize biological macromolecules for rapid proliferation cells; moreover, it contributes maintenance intracellular redox homeostasis producing variety reducing agents. Moreover, derivatives metabolites play critical roles signal transduction within cells tumor microenvironment evades immune destruction facilitates invasion metastasis. These findings suggest close relationship during malignant progression cancers. This review focuses on crosstalk reprogramming, in-depth insight into modulation ROS cancers discusses potential strategies targeting therapy.

Language: Английский

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Galactin-8 DNA methylation mediates macrophage autophagy through the MAPK/mTOR pathway to alleviate atherosclerosis

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 2, 2025

DNA methylation modifications are an important mechanism affecting the process of atherosclerosis (AS). Previous studies have shown that Galectin-8 (GAL8) level is associated with sudden death coronary heart disease or acute events disease. However, GAL8 and gene expression in AS has not been elucidated, prompting us to carry out further research on it. ApoE-/- mice were used establish model, inhibitor DO05 MAPK/mTOR UO126 for intervention. Pyrosequencing was detect changes levels mouse aorta between groups. ROC curve analysis performed assess relationship atherosclerosis. Aortic staining hematoxylin eosin (H&E) observe aortic intima, plaque area, characteristics secondary lesions within plaque. Oil Red O lipid deposition arterial plaques macrophages. Movat number foam cells Immunohistochemistry (IHC) Western blot quantify localization methyltransferase1 (DNMT1), GAL8, pathway proteins, Light Chain3 (LC3), Beclin1, Sequestosome1 (p62), Tumor Necrosis Factor-α (TNF-α), other proteins. Immunofluorescence (IF) fluorescence intensity LC3, Monocyte chemoattractant protein-1(MCP-1), Detection autophagosomes macrophages by transmission electron microscopy also performed. The cell model induced human monocytes (THP-1) co-cultured using siRNAs targeting DO05, UO126. DNMT1 detected blot; red each group, p62, TNF-α quantitatively determined blot. protein, TNF-α, GAL-8 promoter region harbors six CpG sites susceptible methylation. Following inhibition, DC05 group displayed a significant decrease across all compared C57 Conversely, exhibited increased at first three loci relative group. revealed as independent risk factor atherosclerosis: along inflammation-related proteins MCP-1, MMP9, upregulated lesion while autophagy-related LC3 Beclin1 downregulated. Additionally, phosphorylated After inhibiting DNA, up-regulated, macrophage autophagy inhibited, inflammation increased, atherosclerotic aggravated. direct inhibition activity pathway, weakened, inflammatory response aggravated, specific knockdown siRNA cells, above phenomenon reversed, promoted, reduced, degree alleviated. related progression atherosclerosis, its hypomethylation can aggravate lesions. may be through regulation slow down macrophages, then plaques. Targeting new target diagnosis treatment

Language: Английский

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Crosstalk between gut microbiotas and fatty acid metabolism in colorectal cancer

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: Feb. 26, 2025

Abstract Colorectal cancer (CRC) is the third most common malignancy globally and second leading cause of cancer-related mortality. Its development a multifactorial multistage process influenced by dynamic interplay between gut microbiota, environmental factors, fatty acid metabolism. Dysbiosis intestinal microbiota abnormalities in microbiota-associated metabolites have been implicated colorectal carcinogenesis, highlighting pivotal role microbial metabolic interactions. Fatty metabolism serves as critical nexus linking dietary patterns with activity, significantly impacting health. In CRC patients, reduced levels short-chain acids (SCFAs) SCFA-producing bacteria consistently observed. Supplementation probiotics has demonstrated tumor-suppressive effects, while therapeutic strategies aimed at modulating SCFA shown potential enhancing efficacy radiation therapy immunotherapy both preclinical clinical settings. This review explores intricate relationship metabolism, CRC, offering insights into underlying mechanisms their translational applications. Understanding this could pave way for novel diagnostic, therapeutic, preventive management CRC.

Language: Английский

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Inflammatory Bowel Disease: A Comprehensive Analysis of Molecular Bases, Predictive Biomarkers, Diagnostic Methods, and Therapeutic Options

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(13), P. 7062 - 7062

Published: June 27, 2024

In inflammatory bowel diseases (IBDs), such as Crohn's disease (CD) and ulcerative colitis (UC), the immune system relentlessly attacks intestinal cells, causing recurrent tissue damage over lifetime of patients. The etiology IBD is complex multifactorial, involving environmental, microbiota, genetic, immunological factors that alter molecular basis organism. Among these, microbiota cells play pivotal roles; generates antigens recognized by antibodies, while autoantibodies target attack membrane, exacerbating inflammation damage. Given altered framework, analysis multiple biomarkers in patients proves exceedingly valuable for diagnosing prognosing IBD, including markers like C reactive protein fecal calprotectin. Upon detection classification patients, specific treatments are administered, ranging from conventional drugs to new biological therapies, antibodies neutralize molecules tumor necrosis factor (TNF) integrin. This review delves into targets, biomarkers, treatment options, monitoring techniques, and, ultimately, current challenges management.

Language: Английский

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Mangiferin (mango) attenuates AOM-induced colorectal cancer in rat’s colon by augmentation of apoptotic proteins and antioxidant mechanisms

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Jan. 8, 2024

Abstract Mangiferin (MF) is a natural C-glucosylxantone compound that has many substantial curative potentials against numerous illnesses including cancers. The present study's goal to appraise the chemo preventive possessions of MF on azoxymethane (AOM)-mediated colonic aberrant crypt foci (ACF) in rats. Rats clustered into 5 groups, negative control (A), inoculated subcutaneously with normal saline twice and nourished 0.5% CMC; groups B-E injected 15 mg/kg followed by ingestion CMC (B, cancer control); intraperitoneal inoculation 35 5-fluorouracil (C, reference rats) or 30 (D) 60 (E) MF. Results gross morphology colorectal specimens showed significantly lower total ACF incidence MF-treated rats than controls. colon tissue examination increased availability bizarrely elongated nuclei, stratified cells, higher depletion submucosal glands compared treatment caused regulation pro-apoptotic (increased Bax) proteins reduced β-catenin) expression. Moreover, fed had glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) concentrations their homogenates. supplementation down-shifted pro-inflammatory cytokines (transforming growth factor-α interleukine-6) up-shifted anti-inflammatory (interleukine-10) based serum analysis. chemo-protective mechanistic AOM-induced ACF, shown values penetration, could be correlated its positive modulation apoptotic cascade, antioxidant enzymes, inflammatory originating from AOM oxidative stress insults.

Language: Английский

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The role of oxidative stress in the pathogenesis of ocular diseases: an overview

Molecular Biology Reports, Journal Year: 2024, Volume and Issue: 51(1)

Published: March 27, 2024

Language: Английский

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Kynurenines, Neuronal Excitotoxicity, and Mitochondrial Oxidative Stress: Role of the Intestinal Flora

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(3), P. 1698 - 1698

Published: Jan. 30, 2024

The intestinal flora has been the focus of numerous investigations recently, with inquiries not just into gastrointestinal aspects but also pathomechanism other diseases such as nervous system disorders and mitochondrial diseases. Mitochondrial are most common type inheritable metabolic illness caused by mutations nuclear DNA. Despite intensive research, its diagnosis is usually difficult, unfortunately, treating it challenges physicians. Metabolites kynurenine pathway linked to many disorders, depression, schizophrenia, migraine, associated impaired function. includes substances, for instance kynurenic acid quinolinic acid. In this review, we would like show a possible link between metabolites stress in context flora. Furthermore, summarize markers future therapeutic options excitotoxicity oxidative stress.

Language: Английский

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