Ngan An Bui, Dong Yeol Kim, Jiwon Park, Sang-Min Kim, Hyun Jae Sung, Thuy-Duong ThiTran, Quynh T N Nguyen, Inn-Oc Han
언어
영어(ENG)
URL
https://www.earticle.net/Article/A415497
※ 원문제공기관과의 협약기간이 종료되어 열람이 제한될 수 있습니다.
원문정보
초록
영어
Traumatic brain injury (TBI) is known as a functional corruption of the brain caused by a bump or blast to the head when an object hits suddenly or pierces the skull and penetrates brain tissues. There is an urgent need of understanding the pathophysiology following TBI because the morbidity and mortality rates worldwide caused by TBI have remained high throughout decades. In this study, we used a novel model of adult zebrafish to study the molecular and physiological changes following TBI. Using T-maze, on the 3rd-day post-stab-lesion injury (dpi), learning and memory deficits and poor social response were observed. Results from mirror biting and novel tank tests also provided us insight into their defective mobility, explorational, and territorial instincts. Neurogenesis impairment and severe brain inflammation were also altered following TBI, especially at 3 dpi. Upon injury, a notable decrease of O-GlcNAc level was remarked at 3dpi. Deregulation of O-GlcNAcylation which led to impaired glucose metabolism was informed to contribute to the pathologies of neurodegenerative diseases. Glucosamine (GlcN), a natural compound found in cartilage, is known as a derivative of the pathway that can increase O-GlcNAcylation by bypassing the reaction catalyzed by a rate liming enzyme GFAT. To further investigate the correlation, after TBI exposure, zebrafish had been recovered 3 days in 0.1g/L glucosamine (GlcN) diluted in water. Under the treatment of GlcN, the inflammation level reduced significantly, indicated by the decrease of Nuclear factor-kappa B and Glial fibrillary acidic protein expression in the telencephalon. TBI-induced downregulation of the cAMP signaling pathway and its relevant proteins in synaptic plasticity were rescued by GlcN. O-GlcNAc deficiency observed previously, as well as L/M capability were retrieved. GlcN also elevated the number of new cells regenerations and neuronal differentiation. As a result, regulation of brain O-GlcNAcylation may hold a potential role in TBI’s recuperation.
저자
Ngan An Bui [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Dong Yeol Kim [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Jiwon Park [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Sang-Min Kim [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Hyun Jae Sung [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Thuy-Duong ThiTran [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Quynh T N Nguyen [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Inn-Oc Han [ Program in Biomedical Science and Engineering, Inha University, 100 Inha-ro, Michuhol-gu, Incheon 22212, Republic of Korea ]
Corresponding Author
본 학회는 화학, 생화학, 분자생물학, 미생물학, 식품공학, 의학, 약학, 유전공학 및 생물공학, 환경 및 기타 공업 등 전 분야의 탄수화물관련 이론과 기술을 연구 발전시키고 산학협동을 통해 이를 보급하여 국내 관련 산업의 발전 및 국민생활의 과학화에 기여하고자 하며, 이러한 목표와 비젼의 실현을 위해 회원들이 적극적인 참여와 활동을 전개하고자 한다.