Neural Regeneration Research ›› 2019, Vol. 14 ›› Issue (9): 1530-1535.doi: 10.4103/1673-5374.255974

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Sodium butyrate prevents radiation-induced cognitive impairment by restoring pCREB/BDNF expression

Hae June Lee 1 , Yeonghoon Son 1, 2 , Minyoung Lee 3 , Changjong Moon 4 , Sung Ho Kim 4 , In Sik Shin 4 , Miyoung Yang 5 , Sangwoo Bae 1 , Joong Sun Kim 6   

  1. 1 Division of Basic Radiation Bioscience, Korea Institute of Radiological & Medical Sciences (KIRMAS), Seoul, Republic of Korea
    2 National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, Republic of Korea
    3 College of Pharmacy, Kyungpook National University, Daegu, Republic of Korea
    4 College of Veterinary Medicine, Veterinary Medical Research Institute, Chonnam National University, Gwangju, Republic of Korea
    5 School of Medicine, Wonkwang University, Jeonbuk, Republic of Korea
    6 Research Center, Dongnam Institute of Radiological & Medical Sciences (DIRAMS), Busan, Republic of Korea
  • Online:2019-09-15 Published:2019-09-15
  • Contact: Joong Sun Kim, jskim@dirams.re.kr.
  • Supported by:

    This work was supported by the Nuclear Research and Development Program (NRF-2012M2A2A7012377, NRF-2015M2B2B1068627 and NRF-2015R1C1A2A01053041) of the National Research Foundation of Korea (NRF) funded by the Korean Government Ministry of Science, ICT & Future Planning.

Abstract:

Sodium butyrate is a histone deacetylase inhibitor that affects various types of brain damages. To investigate the effects of sodium butyrate on hippocampal dysfunction that occurs after whole-brain irradiation in animal models and the effect of sodium butyrate on radiation exposure-induced cognitive impairments, adult C57BL/6 mice were intraperitoneally treated with 0.6 g/kg sodium butyrate before exposure to 10 Gy cranial irradiation. Cognitive impairment in adult C57BL/6 mice was evaluated via an object recognition test 30 days after irradiation. We also detected the expression levels of neurogenic cell markers (doublecortin) and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor. Radiation-exposed mice had decreased cognitive function and hippocampal doublecortin and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression. Sodium butyrate pretreatment reversed these changes. These findings suggest that sodium butyrate can improve radiation-induced cognitive dysfunction through inhibiting the decrease in hippocampal phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression. The study procedures were approved by the Institutional Animal Care and Use Committee of Korea Institute of Radiological Medical Sciences (approval No. KIRAMS16-0002) on December 30, 2016.

Key words: sodium butyrate, radioprotector, ionizing radiation, hippocampal damage, cAMP response element binding, brain-derived neurotrophic factor, histone deacetylase inhibitor, neurogenesis