亚慢性维生素a缺乏饮食对初生大鼠乳腺细胞凋亡的影响。

2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology
Oxidative Medicine and Cellular Longevity Pub Date : 2025-07-14 eCollection Date: 2025-01-01 DOI:10.1155/omcl/6334165
M Vasquez Gomez, V Filippa, M Acosta, F Mohamed, F Campo Verde, C Ferrari, G A Jahn, M S Giménez, D C Ramirez, S E Gomez Mejiba
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引用次数: 0

摘要

乳腺上皮功能障碍是亚慢性膳食维生素A缺乏(VAD)的严重后果之一。然而,这一过程的潜在机制尚不完全清楚。因此,我们使用了一个原始的饮食性VAD大鼠模型(3个月和6个月),随后在治疗完成前(0.5或1个月)进行了维生素a充足(VAS)饮食的干预。该实验模型使我们能够探讨VAD引起乳腺组织功能障碍的潜在分子机制。饲粮添加VAD 3和6个月可导致乳腺实质和腺细胞炎症细胞浸润增加,炎症和凋亡增加,细胞增殖减少。这些变化可以通过VAS饮食来逆转。NF-κB和维甲酸(RA)信号通路失衡是亚慢性VAD后乳腺功能障碍的基础。饲喂VAD饮食的未生育大鼠由于炎症、细胞凋亡和细胞生长受损而经历乳腺上皮功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Apoptosis in the Mammary Gland of Virgin Rats Subchronically Fed With a Vitamin A Deficient Diet.

Mammary gland epithelial dysfunction is one of the serious consequences of subchronic dietary vitamin A deficiency (VAD). However, the underlying mechanism of this process is incompletely known. Consequently, we utilized a virgin rat model of dietary VAD (3 and 6 months) and subsequently intervened with a vitamin A sufficient (VAS) diet (0.5 or 1 month) prior to treatment completion. This experimental model allowed us to investigate the underlying molecular mechanism of mammary gland tissue dysfunction caused by VAD. Dietary VAD for 3 and 6 months caused increased inflammatory cell infiltration in the mammary gland parenchyma and glandular cells, with increased inflammation and apoptosis and reduced cell proliferation. These changes can be reversed with a VAS diet. Imbalances between the NF-κB and retinoic acid (RA) signaling pathways underlie mammary gland dysfunction following subchronic VAD. Nulliparous rats fed a VAD diet experience mammary gland epithelial dysfunction because of inflammation, apoptosis, and impaired cell growth.

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来源期刊
CiteScore
13.20
自引率
0.00%
发文量
1274
审稿时长
3-8 weeks
期刊介绍: Oxidative Medicine and Cellular Longevity is a unique peer-reviewed, Open Access journal that publishes original research and review articles dealing with the cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, metabolism, cellular survival and cellular longevity. Oxidative stress impacts almost all acute and chronic progressive disorders and on a cellular basis is intimately linked to aging, cardiovascular disease, cancer, immune function, metabolism and neurodegeneration. The journal fills a significant void in today’s scientific literature and serves as an international forum for the scientific community worldwide to translate pioneering “bench to bedside” research into clinical strategies.
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