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限时喂养通过抑制 NOX-4/ROS/p38 MAPK 通路防止电离辐射诱导的造血干细胞损伤。

Time-restricted feeding prevents ionizing radiation-induced hematopoietic stem cell damage by inhibiting NOX-4/ROS/p38 MAPK pathway.

机构信息

Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Science & Peking Union Medical College, Tianjin, China.

Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Science & Peking Union Medical College, Tianjin, China.

出版信息

Int Immunopharmacol. 2024 Mar 30;130:111695. doi: 10.1016/j.intimp.2024.111695. Epub 2024 Feb 23.

DOI:10.1016/j.intimp.2024.111695
PMID:38401461
Abstract

Ionizing radiation (IR)-induced damage to the hematopoietic system is a prominent symptom following exposure to total body irradiation (TBI). The exploration of strategies aimed at to mitigating radiation-induced hematopoietic damage assumes paramount importance. Time-restricted feeding (TRF) has garnered attention for its beneficial effects in various diseases. In this study, we evaluated the preventive effects of TRF on TBI-induced hematopoietic damage. The results suggested that TRF significantly enhanced the proportion and function of hematopoietic stem cells in mice exposed to 4 Gy TBI. These effects might be attributed to the inhibition of the NOX-4/ROS/p38 MAPK pathway in hematopoietic stem cells. TRF also influenced the expression of nuclear factor erythroid2-related factor 2 and increased glutathione peroxidase activity, thereby promoting the clearance of reactive oxygen species. Furthermore, TRF alleviated aberrations in plasma metabolism by inhibiting the mammalian target of rapamycin. These findings suggest that TRF may represent a novel approach to preventing hematopoietic radiation damage.

摘要

电离辐射(IR)对造血系统的损伤是全身照射(TBI)后出现的一个突出症状。探索减轻辐射诱导的造血损伤的策略至关重要。限时喂养(TRF)因其在各种疾病中的有益作用而受到关注。在这项研究中,我们评估了 TRF 对 TBI 诱导的造血损伤的预防作用。结果表明,TRF 可显著提高 4GyTBI 照射小鼠造血干细胞的比例和功能。这些作用可能归因于抑制造血干细胞中的 NOX-4/ROS/p38MAPK 通路。TRF 还影响核因子红细胞 2 相关因子 2 的表达并增加谷胱甘肽过氧化物酶的活性,从而促进清除活性氧。此外,TRF 通过抑制雷帕霉素靶蛋白来减轻血浆代谢的异常。这些发现表明,TRF 可能代表一种预防造血辐射损伤的新方法。

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