Abstract：Objective: To investigate the effect of vitamin D on hypoxic-ischemic brain damage(HIBD) in neonatal rats and its possible mechanism. Methods: A total of 54 neonatal rats were randomly divided into control-48h, control-72h, HIBD-48h, HIBD-72h, treatment-48h and treatment-72h groups, with 9 rats in each group. The HIBD model was established by double ligation of the right common carotid artery. The neonatal rats in the treatment group were treated with vitamin 24 or 48 hours after the establishment of the model, and were killed 24 hours after the drug administration. The neonatal rats in each group were divided into 48h and 72h subgroups. Kits were used to detect the content of 1, 25-dihydroxyvitamin D3 (1,25(OH)2D3), superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in brain tissue. Hematoxylin-eosin (HE) staining was used to detect the neuronal status. RT-qPCR and Western blot were used to detect the mRNA and protein expression of acid sensitive ion channel 1a (ASIC1a) and vitamin D receptor (VDR) genes. Results: With the extension of the model construction time, the content of 1,25(OH)2D3 and SOD activity in the brain of the neonatal rats gradually decreased, the content of MDA increased, the pH value decreased, the mRNA content and protein expression of VDR decreased, and the mRNA content and protein expression of ASIC1a increased. Compared with the control group, the contents of 1,25(OH)2D3 and the activity of SOD in the brain of neonatal rats in the HIBD group were decreased (P<0.05), MDA contents were increased (P<0.05), pH values were decreased (P<0.05), and VDR mRNA and protein expressions were decreased (P<0.05), ASIC1a mRNA and protein expressions were increased (P<0.05). HE staining showed that the neuronal state was obviously damaged. Compared with the HIBD group, the treatment group had increased 1,25(OH)2D3 content and SOD activity in the brain (P<0.05), MDA content decreased (P<0.05), increased pH value (P<0.05), increased VDR mRNA and protein expression (P<0.05), decreased ASIC1a mRNA and protein expression (P<0.05), and HE staining showed that the state of neurons was significantly recovered. Conclusion: Vitamin D can improve neuronal injury in neonatal rats with HIBD by increasing the expression of VDR, restoring brain pH value, reducing the expression of ASIC1a protein, and reducing oxidative stress.
李锋, 韦勇, 万珍玲, 邢凯慧, 吕子栋. 维生素D对缺氧缺血性脑损伤新生大鼠的影响及机制探索[J]. 河北医学, 2025, 31(9): 1439-1446.
LI Feng, WEI Yong, WANG Zhenling, et al. Effect of Vitamin D on Hypoxic-Ischemic Brain Damage in Neonatal Rats and Its Mechanism. HeBei Med, 2025, 31(9): 1439-1446.
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2025, Vol. 31 
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