Chao Zhang , Yue Wang , Fengya Huang , Yaoyuan Zhang , Mingyue Huang , Yunzhu Liu , Linet Angwa , Yanhui Gao , Dianjun Sun , Yuting Jiang
{"title":"氟致血管内皮损伤及蓝莓花青素的保护机制。","authors":"Chao Zhang , Yue Wang , Fengya Huang , Yaoyuan Zhang , Mingyue Huang , Yunzhu Liu , Linet Angwa , Yanhui Gao , Dianjun Sun , Yuting Jiang","doi":"10.1016/j.fct.2025.115665","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Long-term fluoride exposure poses significant risks to the cardiovascular system, with vascular endothelial damage being the critical initiating factor in fluoride induced CVDs. Fluoride's oxidative stress mediated toxicity disrupted endothelial function, highlighting the urgent need for protective strategies. Acy, known for its antioxidant properties, offered potential cardiovascular protection against fluoride induced damage. Previous studies by our group had identified the p53/miR-200c-3p pathway as a key molecular mechanism in fluoride-triggered endothelial injury.</div></div><div><h3>Purpose</h3><div>This study aimed to investigate how fluoride induced vascular endothelial injury and to evaluate the protective role of Acy in counteracting these detrimental effects.</div></div><div><h3>Study design</h3><div>We established both in vivo (fluoride exposed Wistar rats) and in vitro (ECs) models of fluoride toxicity, with Acy intervention.</div></div><div><h3>Results</h3><div>Fluoride exposure caused severe oxidative stress and endothelial dysfunction, which were significantly mitigated by Acy treatment. Notably, Acy alleviated fluoride-induced pathological damage in the vascular endothelium. Mechanistically, Acy exerted its protective effects by suppressing the fluoride-activated p53/miR-200c-3p pathway.</div></div><div><h3>Conclusion</h3><div>Fluoride exposure led to substantial cardiovascular injury, primarily through oxidative stress and endothelial dysfunction. Acy, as a nutritional intervention, effectively counteracted fluoride induced damage, providing novel insights into both the pathogenesis of fluoride toxicity and potential therapeutic strategies for fluorosis.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"204 ","pages":"Article 115665"},"PeriodicalIF":3.5000,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Fluoride-induced vascular endothelial injury and the protective mechanism of blueberry anthocyanins\",\"authors\":\"Chao Zhang , Yue Wang , Fengya Huang , Yaoyuan Zhang , Mingyue Huang , Yunzhu Liu , Linet Angwa , Yanhui Gao , Dianjun Sun , Yuting Jiang\",\"doi\":\"10.1016/j.fct.2025.115665\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Long-term fluoride exposure poses significant risks to the cardiovascular system, with vascular endothelial damage being the critical initiating factor in fluoride induced CVDs. Fluoride's oxidative stress mediated toxicity disrupted endothelial function, highlighting the urgent need for protective strategies. Acy, known for its antioxidant properties, offered potential cardiovascular protection against fluoride induced damage. Previous studies by our group had identified the p53/miR-200c-3p pathway as a key molecular mechanism in fluoride-triggered endothelial injury.</div></div><div><h3>Purpose</h3><div>This study aimed to investigate how fluoride induced vascular endothelial injury and to evaluate the protective role of Acy in counteracting these detrimental effects.</div></div><div><h3>Study design</h3><div>We established both in vivo (fluoride exposed Wistar rats) and in vitro (ECs) models of fluoride toxicity, with Acy intervention.</div></div><div><h3>Results</h3><div>Fluoride exposure caused severe oxidative stress and endothelial dysfunction, which were significantly mitigated by Acy treatment. Notably, Acy alleviated fluoride-induced pathological damage in the vascular endothelium. Mechanistically, Acy exerted its protective effects by suppressing the fluoride-activated p53/miR-200c-3p pathway.</div></div><div><h3>Conclusion</h3><div>Fluoride exposure led to substantial cardiovascular injury, primarily through oxidative stress and endothelial dysfunction. Acy, as a nutritional intervention, effectively counteracted fluoride induced damage, providing novel insights into both the pathogenesis of fluoride toxicity and potential therapeutic strategies for fluorosis.</div></div>\",\"PeriodicalId\":317,\"journal\":{\"name\":\"Food and Chemical Toxicology\",\"volume\":\"204 \",\"pages\":\"Article 115665\"},\"PeriodicalIF\":3.5000,\"publicationDate\":\"2025-07-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Food and Chemical Toxicology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0278691525004338\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"FOOD SCIENCE & TECHNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food and Chemical Toxicology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0278691525004338","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
Fluoride-induced vascular endothelial injury and the protective mechanism of blueberry anthocyanins
Background
Long-term fluoride exposure poses significant risks to the cardiovascular system, with vascular endothelial damage being the critical initiating factor in fluoride induced CVDs. Fluoride's oxidative stress mediated toxicity disrupted endothelial function, highlighting the urgent need for protective strategies. Acy, known for its antioxidant properties, offered potential cardiovascular protection against fluoride induced damage. Previous studies by our group had identified the p53/miR-200c-3p pathway as a key molecular mechanism in fluoride-triggered endothelial injury.
Purpose
This study aimed to investigate how fluoride induced vascular endothelial injury and to evaluate the protective role of Acy in counteracting these detrimental effects.
Study design
We established both in vivo (fluoride exposed Wistar rats) and in vitro (ECs) models of fluoride toxicity, with Acy intervention.
Results
Fluoride exposure caused severe oxidative stress and endothelial dysfunction, which were significantly mitigated by Acy treatment. Notably, Acy alleviated fluoride-induced pathological damage in the vascular endothelium. Mechanistically, Acy exerted its protective effects by suppressing the fluoride-activated p53/miR-200c-3p pathway.
Conclusion
Fluoride exposure led to substantial cardiovascular injury, primarily through oxidative stress and endothelial dysfunction. Acy, as a nutritional intervention, effectively counteracted fluoride induced damage, providing novel insights into both the pathogenesis of fluoride toxicity and potential therapeutic strategies for fluorosis.
期刊介绍:
Food and Chemical Toxicology (FCT), an internationally renowned journal, that publishes original research articles and reviews on toxic effects, in animals and humans, of natural or synthetic chemicals occurring in the human environment with particular emphasis on food, drugs, and chemicals, including agricultural and industrial safety, and consumer product safety. Areas such as safety evaluation of novel foods and ingredients, biotechnologically-derived products, and nanomaterials are included in the scope of the journal. FCT also encourages submission of papers on inter-relationships between nutrition and toxicology and on in vitro techniques, particularly those fostering the 3 Rs.
The principal aim of the journal is to publish high impact, scholarly work and to serve as a multidisciplinary forum for research in toxicology. Papers submitted will be judged on the basis of scientific originality and contribution to the field, quality and subject matter. Studies should address at least one of the following:
-Adverse physiological/biochemical, or pathological changes induced by specific defined substances
-New techniques for assessing potential toxicity, including molecular biology
-Mechanisms underlying toxic phenomena
-Toxicological examinations of specific chemicals or consumer products, both those showing adverse effects and those demonstrating safety, that meet current standards of scientific acceptability.
Authors must clearly and briefly identify what novel toxic effect (s) or toxic mechanism (s) of the chemical are being reported and what their significance is in the abstract. Furthermore, sufficient doses should be included in order to provide information on NOAEL/LOAEL values.