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Abstract

Acid-Sensing Ion Channel 1a Signaling Target and Vitamin D-Mediated Mechanisms in Hypoxic-Ischemic Brain Damage of Neonatal Rat

Author(s): Shenglong Wu, Y. Wei, Z. Lv, Zhenling Wan, Kaihui Xing, F. Li and D. Deng*
Department of Radiology, 1Department of Pathology, 2Department of Neonatology, Hainan Women and Children's Medical Center, Haikou, Hainan Province 570206, 3Department of Radiology, Hainan Modern Women and Children's Hospital, Haikou, Hainan Province 570203, China

Correspondence Address:
D. Deng, Department of Radiology, Hainan Women and Children's Medical Center, Haikou, Hainan Province 570206, China, E-mail: danqiong8@126.com


Roles of acid-sensing ion channel 1a and vitamin D-mediated protective mechanisms in hypoxic-ischemic brain damage of neonatal rat were investigated in this work. 108 Sprague Dawley rats were randomly grouped into a sham operation group (Group A), a hypoxic-ischemic brain damage group (Group B), and a vitamin D treatment group (Group C), with 36 rats in each. A hypoxic-ischemic brain damage rat model was established to assess the blood-brain barrier permeability. Additionally, concentrations of 1,25(OH)2D3, superoxide dismutase activity, malondialdehyde levels, acid-sensing ion channel 1a, as well as vitamin D receptor gene and protein expressions in rat brain tissues were analyzed. Results showed that concentrations of 1,25(OH)2D3 in brain tissues and serum, superoxide dismutase levels, and malondialdehyde levels in Group C were higher in contrast to those in Group B but lower than those in Group A (p<0.05). The pH values in the brain tissues of Group C at 48 h and 72 h were higher than the value in Group B but lower in comparison to the Group A (p<0.05). Blood-brain barrier permeability in Group C was improved. Acid-sensing ion channel 1a was elevated in Group C than that in Group B but decreased than that in Group A (p<0.05). Furthermore, vitamin D receptor in Group B was higher, showing obvious differences to that in Groups A and C (p<0.05). In conclusion, vitamin D supplementation protected hypoxic-ischemic brain damage in rats by enhancing superoxide dismutase activity, downregulating malondialdehyde, regulating acid-base balance, improving blood-brain barrier permeability, and inhibiting acid-sensing ion channel 1a and vitamin D receptor.

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