Nuclear transcription factor κB and cerebral ischemia-reperfusion injury.doc

 PAGE \* MERGEFORMAT 23 Nuclear transcription factor κB and cerebral ischemia-reperfusion injury Keywords: Cerebral ischemia NFkappa B and cerebral ischemia reperfusion Cerebral ischemia-reperfusion injury (CIRI) is excitatory (amino acid) poisoning, oxidative stress, intracellular calcium overload, inflammation and apoptosis (AP) and many other factors are involved in the pathological process [1]. The past, the mechanism of CIRI study focused on oxidative stress, excitatory (amino acid) poisoning, intracellular calcium overload, etc., in recent years with the development of molecular biology and found that CIRI and the inflammatory response and apoptosis are also closely relationship. CIRI in inflammatory cells and inflammatory molecules play a key role, but can regulate transcription of a variety of inflammatory molecules, and can cause increased expression of target genes of nuclear transcription factor κB (NFκB) plays an important role in regulating. At the same time the occurrence of apoptosis after CIRI is an initiative by the gene regulation of cell death process, a variety of gene products expressed in CIRI initiative of cell apoptosis in the course of the protective or injury; In addition, NFκB as a pro-apoptotic factor, or anti-apoptotic factors in different combinations with some combination of CIRI apoptosis-related genes also have different effects. 1 NFκB biological characteristics of 1.1 NFκB structural characteristics of NFκB belongs to Rel family of proteins is determined by two kinds of Rel family subunits: RelA (p65), RelB, cRel, and NFκB1 (p50/p105), NFκB2 (p52) in any two kinds of NFκB / Rel protein subunit of dimer composed of proteins, these proteins all have to work with DNA binding properties, also known as DNA binding subunits, which play a major physiological function of the p50 and p65 proteins constitute a dimer. When the cell is in stationary state, NFκB with its inhibitory protein (Inhibitory Kappa B,