低压缺氧条件下大鼠骨髓红细胞凋亡的机制

IF 2.1 4区 医学 Q3 HEMATOLOGY
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引用次数: 0

摘要

本研究旨在探讨大鼠骨髓中的红细胞在暴露于低压氧后凋亡的机制。雄性 SD 大鼠被随机分为三组。缺氧组分别在模拟海拔 5000 米的低压缺氧箱中饲养 7 天和 28 天。我们发现,与对照组相比,缺氧后髓系:红细胞(M:E)比例明显降低,多色红细胞和正色红细胞比例明显增加,CD71+细胞比例和细胞凋亡率明显增加。低氧暴露后,CD71+细胞中Caspase-3、Bax和Cyt-C的表达水平高于对照组,而TNFR和Fas的表达水平无明显差异。总之,暴露于低压缺氧后,大鼠外周血和骨髓红细胞的增殖增加,凋亡也增加,表明大鼠骨髓红细胞受增殖和凋亡的双重调控,而线粒体途径是凋亡的重要途径之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanism of the apoptosis of bone marrow erythroblasts in rats under hypobaric hypoxia

This study aimed to investigate the mechanism of the apoptosis of erythroblasts in rat bone marrow after the exposure to hypobaric hypoxia. Male SD rats were randomly divided into three groups. The hypoxic group was kept in a hypobaric hypoxia chamber at a simulated altitude of 5000 m for 7 and 28 days, respectively. The control group was kept at an altitude of 2260 m. We found that myeloid: erythroid (M:E) ratio was significantly lower after hypoxia exposure and the proportions of polychromatic erythroblasts and orthochromatic erythroblasts significantly increased compared to control group, along with significant increase in the proportion of CD71+ cells and apoptosis rate. The expression levels of caspase-3, Bax, and Cyt-C in CD71+ cells were higher after hypoxia exposure than those in control group, while there was no significant difference in the expression levels of TNFR and Fas. In conclusion, after exposure to hypobaric hypoxia the proliferation of peripheral blood and bone marrow erythroblasts in rats increased, and apoptosis also increased, indicating that bone marrow erythroblasts in rats is regulated by both proliferation and apoptosis, and the mitochondrial pathway is one of the important pathways for apoptosis.

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来源期刊
CiteScore
4.90
自引率
0.00%
发文量
42
审稿时长
14 days
期刊介绍: Blood Cells, Molecules & Diseases emphasizes not only blood cells, but also covers the molecular basis of hematologic disease and studies of the diseases themselves. This is an invaluable resource to all those interested in the study of hematology, cell biology, immunology, and human genetics.
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