Fluoride-induced vascular endothelial injury and the protective mechanism of blueberry anthocyanins

IF 3.5 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology Pub Date : 2025-07-29 DOI:10.1016/j.fct.2025.115665

Chao Zhang , Yue Wang , Fengya Huang , Yaoyuan Zhang , Mingyue Huang , Yunzhu Liu , Linet Angwa , Yanhui Gao , Dianjun Sun , Yuting Jiang

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Abstract

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.

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氟致血管内皮损伤及蓝莓花青素的保护机制。

背景：长期氟化物暴露对心血管系统有重大风险，血管内皮损伤是氟化物诱发心血管疾病的关键启动因素。氟化物的氧化应激介导的毒性破坏内皮功能，强调迫切需要保护策略。Acy以其抗氧化特性而闻名，对氟化物引起的心血管损伤提供了潜在的保护。我们课组之前的研究已经发现p53/miR-200c-3p通路是氟化物引发内皮损伤的关键分子机制。目的：探讨氟化物诱导血管内皮损伤的机制，并评价其在对抗这些损伤中的保护作用。研究设计：我们在Acy干预下建立了体内（氟暴露Wistar大鼠）和体外（ECs）氟化物毒性模型。结果：氟暴露引起严重的氧化应激和内皮功能障碍，Acy治疗可显著减轻这一影响。值得注意的是，Acy减轻了氟化物引起的血管内皮病理损伤。机制上，Acy通过抑制氟化物激活的p53/miR-200c-3p通路发挥其保护作用。结论：氟暴露主要通过氧化应激和内皮功能障碍导致大量心血管损伤。Acy作为一种营养干预手段，可以有效地抵消氟化物引起的损伤，为氟化物中毒的发病机制和氟中毒的潜在治疗策略提供了新的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Food and Chemical Toxicology 工程技术-毒理学

CiteScore

10.90

自引率

4.70%

发文量

651

审稿时长

31 days

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.