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多囊卵巢综合征大鼠模型中维生素 D 状态对主动脉血管功能的影响。

Effect of Vitamin D Status on Vascular Function of the Aorta in a Rat Model of PCOS.

机构信息

Department of Obstetrics and Gynecology, Semmelweis University, Hungary Budapest, Üllői út 78/a, H-1082.

Department of Obstetrics and Gynecology, Markusovszky Lajos University Teaching Hospital, Hungary Szombathely, Markusovszky Lajos utca 5., H-9700.

出版信息

Oxid Med Cell Longev. 2021 Mar 18;2021:8865979. doi: 10.1155/2021/8865979. eCollection 2021.

DOI:10.1155/2021/8865979
PMID:33791074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7997742/
Abstract

Polycystic ovary syndrome (PCOS) is associated with elevated cardiovascular risk. Early vascular dysfunction may lead to the development of cardiovascular disease in PCOS. Vitamin D deficiency (VDD) is a common comorbidity of PCOS that contributes to the pathogenesis of the disease and its complications. Both PCOS and VDD are accompanied by increased oxidative stress that may be involved in the arising vascular dysfunction. We aimed to investigate the role of vitamin D status on aortic function. PCOS was induced by an 8-week-long transdermal testosterone treatment of female rats, and low and adequate vitamin D status was achieved by dietary means. Contraction and relaxation abilities of isolated aortic segments were measured by myograph. Resorcin-fuchsin staining and immunohistochemical labeling of 3-nitrotyrosine were performed. No difference was shown in the norepinephrine-induced contraction of the aortas of different groups, whereas we detected reduced acetylcholine- and insulin-evoked relaxation in VDD groups. A lower level of resorcin-fuchsin staining and elevated 3-nitrotyrosine immunostaining was observed in VDD. In our study, we demonstrated early endothelial dysfunction in VDD PCOS rat model. Vitamin D supplementation could prevent vascular disturbances, while VDD itself damaged endothelium-dependent vasorelaxation and induced nitrative stress.

摘要

多囊卵巢综合征(PCOS)与心血管风险升高有关。早期血管功能障碍可能导致 PCOS 患者发生心血管疾病。维生素 D 缺乏(VDD)是 PCOS 的常见合并症,会导致疾病的发病机制及其并发症的发生。PCOS 和 VDD 都会导致氧化应激增加,这可能与血管功能障碍的发生有关。我们旨在研究维生素 D 状态对主动脉功能的影响。通过对雌性大鼠进行为期 8 周的透皮睾酮治疗来诱导 PCOS,通过饮食来实现低和足够的维生素 D 状态。通过肌动描记法测量分离的主动脉段的收缩和舒张能力。进行间苯二酚-品红染色和 3-硝基酪氨酸的免疫组织化学标记。不同组的去甲肾上腺素诱导的主动脉收缩没有差异,但我们发现 VDD 组的乙酰胆碱和胰岛素诱导的舒张减少。VDD 组的间苯二酚-品红染色水平较低,3-硝基酪氨酸免疫染色水平升高。在我们的研究中,我们在 VDD PCOS 大鼠模型中证明了早期的内皮功能障碍。维生素 D 补充可以预防血管紊乱,而 VDD 本身会损害内皮依赖性血管舒张并诱导硝化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b642/7997742/cc86d9cc1f35/OMCL2021-8865979.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b642/7997742/14aa23472126/OMCL2021-8865979.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b642/7997742/cc86d9cc1f35/OMCL2021-8865979.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b642/7997742/14aa23472126/OMCL2021-8865979.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b642/7997742/cc86d9cc1f35/OMCL2021-8865979.002.jpg

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3
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4
The effects of vitamin D on cardiovascular damage induced by lipopolysaccharides in rats.维生素D对大鼠脂多糖诱导的心血管损伤的影响。
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5
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6
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7
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8
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9
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