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Effects of hyperbaric oxygen on Notch signaling pathway after severe carbon monoxide poisoning in mice
Hui-Jun Hu1, Dan-Feng Fan1, Zhou-Heng Ye2, Qiang Sun1
1 Department of Hyperbaric Medicine, the Sixth Medical Center, Chinese PLA General Hospital, Beijing, China
2 Department of Special Operations Medicine, the Sixth Medical Center, Chinese PLA General Hospital, Beijing, China
Correspondence Address:
Qiang Sun,
Department of Hyperbaric Medicine, the Sixth Medical Center, Chinese PLA General Hospital, Beijing
China
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/2045-9912.344971
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Demyelination of the cerebral white matter is the most common pathological change after carbon monoxide (CO) poisoning. Notch signaling, the mechanism underlying the differentiation of astrocytes and oligodendrocytes, is critical to remyelination of the white matter after brain lesion. The purpose of this work was to determine the effects of hyperbaric oxygen (HBO) on Notch signaling pathway after CO poisoning for the explanation of the protective effects of HBO on CO-poisoning-related cerebral white matter demyelination. The male C57 BL/6 mice with severe CO poisoning were treated by HBO. And HBO therapy shortened the escape latency and improved the body mass after CO poisoning. HBO therapy also significantly suppressed protein and mRNA levels of Notchl and Hes5 after CO poisoning. Our findings suggested that HBO could suppress the activation of Notch signaling pathway after CO poisoning, which is the mechanism underlying the neuroprotection of HBO on demyelination after severe CO poisoning.
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