Pharmaceutical biology · 2026
CB001 bioactive compounds mitigate intestinal immune dysregulation induced by simulated microgravity and radiation via B cells modulation.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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История · было → стало
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Liu Jinfeng, Bai Zhijie, Dong Yang, Wang Yuxin, Li Jiamiao, Wang Ningning, Wang Xizheng, Guo Jie, Zhou Wei, Gao Yue, Wang Xiaoying
Аннотация
BACKGROUND: Gastrointestinal discomfort is a prevalent issue during spaceflight, yet targeted therapeutic strategies remain elusive. Existing research largely relies on single-factor modeling, limiting a comprehensive understanding of the underlying pathologies.
METHODS: We established a composite mouse model combining simulated microgravity (hindlimb unloading) and low-dose radiation (Cobalt-60) to evaluate intestinal injury and the therapeutic potential of CB001. Mechanisms were investigated through histological analysis, in vitro co-culture assays, and flow cytometry assessment of B-cell dynamics and IgA/IgG secretion.
RESULTS: The dual-factor model more effectively simulated spaceflight-induced injuries than single-factor models, showing significant intestinal inflammation and homeostasis disruption. Mechanistically, dual factors promoted CCR7+ B cells migration into the intestine by upregulating CXCR4 expression, subsequently enhancing leukocyte activation. CB001 treatment mitigated these intestinal perturbations by restoring tight junction proteins, suppressing excessive B-cell migration, and downregulating pro-inflammatory cytokines. Furthermore, in vitro assays confirmed that CB001 directly enhanced B-cell viability and augmented IgA/IgG secretion, thereby promoting mucosal repair.
CONCLUSION: CB001 is a promising candidate for mitigating spaceflight-induced intestinal dysfunction, as identified using a novel dual-factor mouse model. These data shed light on strategies for screening protective medicines to safeguard astronaut health during space missions.
METHODS: We established a composite mouse model combining simulated microgravity (hindlimb unloading) and low-dose radiation (Cobalt-60) to evaluate intestinal injury and the therapeutic potential of CB001. Mechanisms were investigated through histological analysis, in vitro co-culture assays, and flow cytometry assessment of B-cell dynamics and IgA/IgG secretion.
RESULTS: The dual-factor model more effectively simulated spaceflight-induced injuries than single-factor models, showing significant intestinal inflammation and homeostasis disruption. Mechanistically, dual factors promoted CCR7+ B cells migration into the intestine by upregulating CXCR4 expression, subsequently enhancing leukocyte activation. CB001 treatment mitigated these intestinal perturbations by restoring tight junction proteins, suppressing excessive B-cell migration, and downregulating pro-inflammatory cytokines. Furthermore, in vitro assays confirmed that CB001 directly enhanced B-cell viability and augmented IgA/IgG secretion, thereby promoting mucosal repair.
CONCLUSION: CB001 is a promising candidate for mitigating spaceflight-induced intestinal dysfunction, as identified using a novel dual-factor mouse model. These data shed light on strategies for screening protective medicines to safeguard astronaut health during space missions.