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Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injury
Soo Young Choi 1,* (Professor), Jung Hwan Park1 (Research worker), Dae Won Kim2 (Research worker), Min Jea Shin1 (Research worker), Jinseu Park1 (Research worker), Kyu Hyung Han1 (Research worker), Keun Wook Lee1 (Research worker), Jong Kook Park1 (Research worker), Yeon Joo Choi1 (Research worker), Hyeon Ji Yeo1 (Research worker), Eun Ji Yeo1 (Research worker), Eun Jeong Sohn1 (Research worker), Hyoung-Chun Kim3 (Research worker), Eun-Joo Shin3 (Research worker), Sung-Woo Cho4 (Research worker)
1Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea,
2Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung 25457, Korea,
3Neuropsychopharmacology and Toxicology Program, BK21 PLUS Project, College of Pharmacy, Kangwon National University, Chunchon, 24341, Korea,
4Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, Korea,
5Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan-Si 31538, Korea. 6Department of Neurosurgery, Hallym University Medical Center, Chuncheon 24253, Korea
Abstract
It is well known that oxidative stress participates in neuronal cell death caused production of reactive oxygen species (ROS). The increased ROS is a major contributor to the development of ischemic injury. Indoleamine 2,3-dioxygenase 1 (IDO-1) is involved in the kynurenine pathway in tryptophan metabolism and plays a role as an anti-oxidant. However, whether IDO-1 would inhibit hippocampal cell death is poorly known. Therefore, we explored the effects of cell permeable Tat-IDO-1 protein against oxidative stress-induced HT-22 cells and in a cerebral ischemia/reperfusion injury model. Transduced Tat-IDO-1 reduced cell death, ROS production, and DNA fragmentation and inhibited mitogen-activated protein kinases (MAPKs) activation in H2O2 exposed HT-22 cells. In the cerebral ischemia/reperfusion injury model, Tat-IDO-1 transduced into the brain and passing by means of the blood-brain barrier (BBB) significantly prevented hippocampal neuronal cell death. These results suggest that Tat-IDO-1 may present an alternative strategy to improve from the ischemic injury.
Abstract, Accepted Manuscript(in press) [Submitted on May 28, 2020, Accepted on June 30, 2020]
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