Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injuryopen access
- Authors
- Park, Jung Hwan; Kim, Dae Won; Shin, Min Jea; Park, Jinseu; Han, Kyu Hyung; Lee, Keun Wook; Park, Jong Kook; Choi, Yeon Joo; Yeo, Hyeon Ji; Yeo, Eun Ji; Sohn, Eun Jeong; Kim, Hyoung-Chun; Shin, Eun-Joo; Cho, Sung-Woo; Kim, Duk-Soo; Cho, Yong-Jun; Eum, Won Sik; Choi, Soo Young
- Issue Date
- 30-Nov-2020
- Publisher
- 생화학분자생물학회
- Keywords
- Ischemia; MAPKs; Oxidative stress; Protein therapy; Tat-IDO-1
- Citation
- BMB Reports, v.53, no.11, pp 582 - 587
- Pages
- 6
- Journal Title
- BMB Reports
- Volume
- 53
- Number
- 11
- Start Page
- 582
- End Page
- 587
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/2309
- DOI
- 10.5483/BMBRep.2020.53.11.114
- ISSN
- 1976-6696
1976-670X
- 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.
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Collections - College of Medicine > Department of Anatomy > 1. Journal Articles
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