Earticle

초록

영어

The proinflammatory cytokines, IL-1β and TNF-α, are known to play a key role in inflammatory reaction in many forms of acute and chronic neurological diseases. In Parkinson’s disease (PD), those cytokines immunoreactivity was significantly increased in the substantia nigra and striatum. Moreover, it is implicated that the production of those cytokines from activated microglial cells in Parkinson’s brain contributes to the increase of pathological oxidative stress. However, it is not clear what is the molecular mechanism of cytokines-related dopaminergic cell death underlying PD. Of interest, treatment with IL- 1β and TNF-α induced minimal cell death when compared with other PD-related neurotoxicants. Although IL-1β induced a transient increase in reactive oxygen species (ROS) production within an hour, TNF-α did not increase ROS production even within 12 hours in dopaminergic neurons. The transcription factor, NF-κB was translocated into nucleus in response to IL-1β prior to ROS increase in dopaminergic cells. In addition, IL-1β activated the JNK 1/2 moderately in dopaminergic neurons and triggered the dopaminergic cell death.

키워드

저자

• Hong Sung CHUN [ Dept. of Biotechnology, Chosun University ]

참고문헌

발행기관

간행물

표지보기 관심저널 등록

• 간행물명

  한국생물공학회 학술대회

• 간기

  반년간

• 수록기간

  1985~2013

• 십진분류

  KDC 476 DDC 576