The molecular mechanism of liver injury.docVIP

 PAGE \* MERGEFORMAT 15 The molecular mechanism of liver injury Authors: WANG Jiao, MENG Wei-hong, Wang Qiang, YAN Wei-Qun [Keywords:] liver injury With regard to the mechanism of liver injury and its prevention and control research at home and abroad in recent years has become a biology, medical research, one of the hot spots [1 ~ 3]. This review in recent years, the molecular mechanism of liver injury related to domestic and international literature review as follows. 1 TNF-induced liver cell injury TNF-α is a major by macrophages produced cytokines. TNF-α for different cell types play a different role in many important pathological and physiological conditions of existence as an important medium [4]. TNF-α is an important mediator of apoptosis. The biological effects of TNF primarily by TNF-R1-mediated [5,6]. TNF-R1 intracellular domain, including death, by activating the nuclear transcription factor NF-κ B certain cell proliferation, differentiation, may also trigger signal transduction cascades which lead to apoptosis. Combination of TNF and TNF-R1 is available through the following three ways to trigger cell death: (1) one way (TNF TNF-R1-TRADD-FADD): TNF and TNF-R1 binding and to TNF-R1 intracellular 3 dimerization, The latter connected with TRADD [7]. TRADD contains a C-terminal death domain (195 ~ 305 amino acid residues), and its connection with TNF-R1 death domain has a high degree of homology. TRADD’s death domain can also with FADD and TRAF2 (TNF receptor-associated factor 2) connection, give rise to different biological effects. (2) Article 2 channels (TNF TNF-R1-TRADD-RIP): TNF and TNF-R1 binding, through TRADD gathered RIP (Receptor-interacting protein) [8]. RIP is a protein kinase molecule, containing 671 amino acids, molecular weight 76000 Dalton. N terminal kinase domain containing 1, C-side with a dead zone. Priority areas of his death combined with the TRADD death domain and TNFR1 occurs with weaker connections. RIP In addition t