摘 要：摘 要：近年来在危重病监护方面有重大的进展，但是脓毒症仍有很高的发病率和死亡率[1]，其本质是由于感染所致机体过度反应，引发炎症因子的过度分泌而引起的促、抗炎因子平衡失调。脂多糖(lipopolysaccharide, LPS)是引起脓毒症的重要因素之一，它可以激活细胞内多条信号转导通路。丝裂原活化蛋白激酶(mitogen-activated protein kinase, MAPK)信号转导途径是体内重要的信号转导通路，参与调节胚胎发育、细胞分化、细胞增殖和细胞死亡，其中MAPK家族中的p38与炎症反应有着密切关系。本文着重综述p38的分子结构、p38信号转导通路的激活、p38的底物以及在由脂多糖激活的脓毒症中p38发挥的重要作用和应用p38抑制剂的防治前景。
关键词：p38；脓毒症；信号转导；转录因子；抑制剂
中图分类号：Q555.7 文献标识码：A
Abstract:
Abstract: Although recently intensive care makes great progress, the incidence and the mortality of sepsis remain very high. The essence is that organism抯 excessive inflammation action by infect results in inflammation cytokine excessive secretion, so that the balance of pro and anti inflammation is broken. Lipopolysaccharide is one of the critical reasons of evoking sepsis, it can activate several cell signal transduction pathsways in vivo. Mitogen-activated protein kinase (MAPK), which is one of the important signal transduction systems in organisms, is involved in many cellular processes, such as embryonic development, cell development, division, differentiation, death, especially p38 has the close relation with inflammation. This article focuses on molecular constitution of p38, activation of p38 signal transcription way, p38 substrate and the effect of sepsis pathogensis and development by LPS, the perspective prevention and treatment of inflammation by specific inhibitors.
Key words: p38; sepsis; signal transcription; transcriptional factor; inhibitor
