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氘消耗对体内随年龄下降的胸腺生成的影响。

Effects of Deuterium Depletion on Age-Declining Thymopoiesis In Vivo.

作者信息

Yaglova Nataliya V, Obernikhin Sergey S, Timokhina Ekaterina P, Tsomartova Dibakhan A, Yaglov Valentin V, Nazimova Svetlana V, Tsomartova Elina S, Ivanova Marina Y, Chereshneva Elizaveta V, Lomanovskaya Tatiana A

机构信息

Laboratory of Endocrine System Development, A.P. Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution "Petrovsky National Research Centre of Surgery", 119991 Moscow, Russia.

Department of Human Anatomy and Histology, Federal State Funded Educational Institution of Higher Education I.M. Sechenov First Moscow State Medical University, 119435 Moscow, Russia.

出版信息

Biomedicines. 2024 Apr 25;12(5):956. doi: 10.3390/biomedicines12050956.

DOI:10.3390/biomedicines12050956
PMID:38790918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11117614/
Abstract

The thymus provides maturation and migration of T cells to peripheral organs of immunity, where they recognize diverse antigens and maintain immunological memory and self-tolerance. The thymus is known to be involved with age and in response to stress factors. Therefore, the search for approaches to the restoration of thymopoiesis is of great interest. The present investigation was aimed at evaluating how prolonged deuterium depletion affects morphogenetic processes and the physiological transition of the thymus to age-related involution. The study was performed on 60 male Wistar rats subjected to consumption of deuterium-depleted water with a 10 ppm deuterium content for 28 days. The control rats consumed distilled water with a normal deuterium content of 150 ppm. The examination found no significant differences in body weight gain or the amount of water consumed. The exposed rats exhibited similar to control dynamics of the thymus weight but significant changes in thymic cell maturation according to cytofluorimetric analysis of thymic subpopulations. Changes in T cell production were not monotonic and differentially engaged morphogenetic processes of cell proliferation, differentiation, and migration. The reactive response to deuterium depletion was a sharp increase in the number of progenitor CD4CD8 cells and their differentiation into T cells. The compensatory reaction was inhibition of thymopoiesis with more pronounced suppression of differentiation of T-cytotoxic lymphocytes, followed by intensification of emigration of mature T cells to the bloodstream. This period lasts from 3 to 14 days, then differentiation of thymic lymphocytes is restored, later cell proliferation is activated, and finally the thymopoiesis rate exceeds the control values. The increase in the number of thymic progenitor cells after 3-4 weeks suggests consideration of deuterium elimination as a novel approach to prevent thymus involution.

摘要

胸腺为T细胞提供成熟和迁移至外周免疫器官的条件,在这些外周免疫器官中,T细胞识别各种抗原并维持免疫记忆和自身耐受性。已知胸腺会随着年龄增长以及对应激因素产生反应。因此,寻找恢复胸腺生成的方法备受关注。本研究旨在评估长期氘消耗如何影响胸腺的形态发生过程以及胸腺向与年龄相关的退化的生理转变。该研究对60只雄性Wistar大鼠进行,让它们饮用氘含量为10 ppm的贫氘水,持续28天。对照大鼠饮用氘含量正常为150 ppm的蒸馏水。检查发现体重增加或饮水量方面无显著差异。暴露组大鼠的胸腺重量动态与对照组相似,但根据胸腺亚群的细胞荧光分析,胸腺细胞成熟出现了显著变化。T细胞生成的变化并非单调,且在细胞增殖、分化和迁移的形态发生过程中存在差异。对氘消耗的反应是祖细胞CD4CD8数量急剧增加并分化为T细胞。补偿反应是胸腺生成受到抑制,T细胞毒性淋巴细胞的分化受到更明显的抑制,随后成熟T细胞向血液中的迁移加剧。这个阶段持续3至14天,然后胸腺淋巴细胞的分化恢复,随后细胞增殖被激活,最终胸腺生成率超过对照值。3至4周后胸腺祖细胞数量增加,这表明可将消除氘视为预防胸腺退化的一种新方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/34c836b259b2/biomedicines-12-00956-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/1ced6bbd49a9/biomedicines-12-00956-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/a4d4d2319ae9/biomedicines-12-00956-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/5e34a0d1ab44/biomedicines-12-00956-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/d116d896d89b/biomedicines-12-00956-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/3f5dbfe26565/biomedicines-12-00956-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/8b04836c2153/biomedicines-12-00956-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/15516bfa7406/biomedicines-12-00956-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/34c836b259b2/biomedicines-12-00956-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/1ced6bbd49a9/biomedicines-12-00956-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/a4d4d2319ae9/biomedicines-12-00956-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/5e34a0d1ab44/biomedicines-12-00956-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/d116d896d89b/biomedicines-12-00956-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/3f5dbfe26565/biomedicines-12-00956-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/8b04836c2153/biomedicines-12-00956-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/15516bfa7406/biomedicines-12-00956-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a6b/11117614/34c836b259b2/biomedicines-12-00956-g008.jpg

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