Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injury

• Published in: BMB reports 2020-11, Vol.53 (11), p.582-587
• Main 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
• Format: Article
• Language: Korean
• Subjects: Ischemia; MAPKs; Oxidative stress; Protein therapy; Tat-IDO-1
• ISSN: 1976-6696; 1976-670X

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. [BMB Reports 2020; 53(11): 582-587]