Studies have shown that vitamin D plays a crucial role in brain development, brain metabolism and neuroprotection. There is little evidence for the neuroprotective effect of 1, 25‑dihydroxyvitamin D3 (1,25‑(OH)2D3) on various brain injury models. The aim of this study was to investigate the neuroprotection effect of 1,25‑(OH)2D3 against hyperoxia‑induced brain injury in premature rats. Sprague‑Dawley rats were exposed to 95% oxygen or room air for 24 h and treated with 1,25‑(OH)2D3 or normal saline for 14 consecutive days. The histopathological changes of optic chiasma tissue were observed by hematoxylin‑eosin staining. Immunohistochemistry, qRT‑PCR, and western blot were performed to detect the expression of integrin‑β1 and yes‑associated protein (YAP) in the organization of the optic chiasm. Histopathological sections of optic chiasma showed visible optic nerve swelling, expanded nerve fiber space, uneven staining, obvious oligodendrocyte proliferation and disordered cell arrangement accompanied by inflammatory cell infiltration and exudation after 7 days and 14 days of hyperoxia exposure. The hyperoxia group treated with 1,25‑(OH)2D3 were showed improvement of brain injury with reduced inflammatory exudation, uniform nerve fiber staining and less obvious oligodendrocyte proliferation. Immunohistochemical staining, qRT‑PCR and western blot indicated that 1,25‑(OH)2D3 treatment upregulated the expression of integrin‑β1 and YAP in the hyperoxia group on day 7. However, the expression of YAP was significantly increased compared with control group and treatment with 1,25‑(OH)2D3 reduced the expression of YAP in the hyperoxic group on day 14. 1,25‑(OH)2D3 may regulate the expression of integrin‑β1 and YAP to alleviate hyperoxia‑induced brain injury in premature rats.
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