Abstract

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.