胰岛素对内毒素诱导大鼠肝细胞损伤的保护作用及其抗炎机制

发布时间：2018-04-14 08:50

本文选题：胰岛素 + 肝细胞　；参考：《第四军医大学》2006年硕士论文

【摘要】：研究背景严重创伤、全身感染、肝病以及众多的危重疾病在其发生发展过程中都可发生肠源性内毒素血症，大量的内毒素可直接或者通过激活肝组织中的枯否细胞(Kupffer cell，KC)合成及释放多种炎性介质间接损伤肝细胞，从而加剧肝脏病变，导致肝功能不全，引发肝衰竭，造成不可逆损伤。临床研究发现，对于重症监护以及烧伤、脓毒血症及感染性休克等危重疾病患者给予胰岛素强化治疗可改善病人症状，降低病人死亡率及其合并症的发生率，但其作用机制尚不清楚。近年发现，，胰岛素不仅可影响细胞糖代谢，还可抑制氧化应激和缺血／再灌注(myocardial ischemia／reperfusion，MI／R)诱导的心肌细胞凋亡，进而发挥心脏保护作用。我室前期的研究也发现在离体细胞和整体动物MI／R模型上胰岛素可通过抗凋亡作用减轻心肌细胞及内皮细胞损伤。新近的研究报道胰岛素能够通过促进肝细胞增殖和抑制肝细胞凋亡，改善肝功能和维持肝脏的完整性。近年来，人们通过对内毒素血症及热损伤大鼠
[Abstract]:Research backgroundSevere trauma, systemic infection, liver disease, and many critical diseases can develop enterogenous endotoxemia during their development.A large amount of endotoxin can directly or by activating Kupffer cell KC) synthesis and release a variety of inflammatory mediators indirectly damage liver cells, thereby exacerbating liver disease, leading to liver failure, liver failure and irreversible damage.Clinical studies have found that intensive insulin therapy for patients with critical diseases such as burns, sepsis and septic shock can improve symptoms, reduce mortality and the incidence of complications.However, the mechanism of its action is not clear.In recent years, it has been found that insulin not only affects glucose metabolism, but also inhibits myocardial cell apoptosis induced by oxidative stress and ischemia / reperfusion myocardial ischemia / reperfusion, thus exerting cardioprotective effect.In vitro and in vivo animal MI/R models, insulin can attenuate the injury of cardiomyocytes and endothelial cells by anti-apoptotic effect.Recent studies have reported that insulin can improve liver function and maintain hepatic integrity by promoting hepatocyte proliferation and inhibiting hepatocyte apoptosis.In recent years, endotoxemia and heat injury in rats
【学位授予单位】：第四军医大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R363

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