Nuclear factor κB - a new focus of acute lung inj

e707004304 · Wysłany: Nie 23:51, 13 Mar 2011

Nuclear factor κB - a new focus of acute lung injury gene therapy

1. InvolvenentofNF-k India paBinsili-ca-inducedcyclooxygenaseIIgeneexpressioninratalveolarnlac-rophages. AmJPhysiol. 1997. 272 (4pt1): L779-786.14YuSM, WuJF. nn. rL. eta1. InhibitionofnitricoxidesynthaseexpressionbyPPM a 18. anovelanti-inflanmmtoryagent, invitroandinvivo. BiochemJ, 1997,328 (pt2) :363-369 .15 I. enlschAB. ShanleyTP, SarmaV, eta1. InvivosuppressionofNF-KBandpreseroationofIKB2byintedeukin a 10andinterleukin-13. JClinInvest, 1997,100 (10) :2443-2448 .16 EscofferN, BoichotE. GermainN. eta1. Effectsofinterleukin-10andmodulatorsofcyclicAMPformationonendotoxin-inducedin-flammationinratlung. FundamClinPharmacol. 1999. 13 (1) :96-101 .17 ReinhartPG. GuptaSK. BhaIlaDK. Atteanationofonme-indueedlunginjurybyinterleukin a 10. ToxicolLett. 1999. l10 (1-2): 3542.18DrazanKE, WuL. BullingtonD. eta1. Viral Ⅱ, 10genetherapyinhibitsTNF-alphaandIL-lbeta. notIIA5, inthenewbomendotox-cmicmouse. JPediatrSurg, 1999,31 (3): 41l4l4. HSP expression in the inflammatory response syndrome in the role and significance of Anesthesiology, Shanghai Sixth People's Hospital (200233) Summary of Jiang Wei,[link widoczny dla zalogowanych], Zhao Gang hide summary revision of heat shock proteins (HSPs) is the organism in the face of adverse living environment for the expression of a rapidly protective protein class family, with repair and maintenance of cell function. In the inflammatory response syndrome (sIRs) pathological process, the body cells were HSP expression, and through molecular chaperone,[link widoczny dla zalogowanych], anti-apoptotic and anti-inflammatory mechanisms play a protective role. This HSP expression in different tissues and outcome of the significance of the development of SIRS are reviewed. Key words Heat shock protein; heat stress response; inflammatory response syndrome; mechanism of systemic inflammatory response syndrome (sIRS) by infection or infection (such as trauma, shock), and other risk factors acting on the body caused by an excessive inflammatory state, leading to excessive release of inflammatory mediators, tissue hypoperfusion and reperfusion injury, or even multiple organ failure. Noxious stimulation in this pathological process, while the body cells induced synthesis of a protein that is highly conserved heat shock protein (heatstressprotein, HSP) to counter the stress factors of the damage. In this paper, Pathological HSP on the SIPS injury and expression in different cells in the pathogenesis of S meaning interventions are summarized below. 1lISP classification and synthesis of HSP's that stems from living cells after the heat tolerance of heat stress response phenomena. The first thing that a certain temperature, heat shock, the cells change gene expression through synthesis of a series of protein molecules that HSP, in order to protect itself from thermal damage. According to molecular weight, HSP can be divided into HSP90 (80-90kD), HSPT0 (66-78kD),[link widoczny dla zalogowanych], HSP60 and small lISP4 a family. HSP70 family, the most important of which are distributed in various cells and has a wide range of cell protection. In addition to high temperature,[link widoczny dla zalogowanych], in the case of arsenic, endotoxin,[link widoczny dla zalogowanych], inflammation, lack of