Drug-Induced Neuroprotection From Global Ischemia Is Associated With Prevention of Persistent but Not Transient Activation of Nuclear Factor-κB in Rats | Zendy

James A. Clemens | Zendy; Diane Stephenson | Zendy; Tinggui Yin | Zendy; E. Barry Smalstig | Zendy; Jill A. Panetta | Zendy; Sheila P. Little | Zendy

Open Access

Drug-Induced Neuroprotection From Global Ischemia Is Associated With Prevention of Persistent but Not Transient Activation of Nuclear Factor-κB in Rats

Author(s) -

James A. Clemens,

Diane Stephenson,

Tinggui Yin,

E. Barry Smalstig,

Jill A. Panetta,

Sheila P. Little

Publication year - 1998

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/01.str.29.3.677

Subject(s) - medicine , neuroprotection , ischemia , drug , pharmacology , transient (computer programming) , stroke (engine) , anesthesia , mechanical engineering , computer science , engineering , operating system

Nuclear factor-kappaB (NF-kappaB) is an oxidative stress responsive transcription factor that is transiently activated in most forebrain neurons in response to transient global ischemia. However, in hippocampal CA1 neurons destined to die, NF-kappaB remains persistently activated. The present study was performed to determine whether an antioxidant (LY231617) that afforded neuroprotection in previous studies had any effect on NF-kappaB activation in hippocampal CA1 neurons after global ischemia.

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