论文部分内容阅读
目的探讨核转录因子κB(NFκB)活化对急性肺损伤(ALI)大鼠P选择素、细胞间黏附分子1(ICAM1)表达的影响,并观察低分子肝素(LMWH)和阿司匹林(ASA)对ALI的保护作用,并探讨其机制。方法尾静脉注射内毒素制备ALI大鼠模型。60只大鼠按随机数字表法分为正常对照组、ALI组、LMWH组和ASA组,每组15只。观察NFκB、ICAM1和P选择素在肺组织中的表达情况。结果ALI组肺组织NFκB活性显著增强;ICAM1、P选择素明显表达于血管内皮细胞和支气管上皮细胞膜(P均<0.05);LMWH组和ASA组NFκB、ICAM1、P选择素活性降低,炎症反应和病理损伤明显减轻,ASA组治疗效果优于LMWH组(P均<0.05)。结论NFκB活化在ALI发病机制中起作用,NFκB参与活化中性粒细胞、血管内皮细胞等多种炎症细胞,并且调控ICAM1、P选择素基因的表达进而造成肺组织损伤。LMWH通过改善微循环,间接抑制NFκB活化,减少中性粒细胞及血小板的黏附进而减轻肺损伤。ASA通过抗氧化特性直接抑制NFκB活化而减轻肺损伤。
Objective To investigate the effect of nuclear factor kappa B (NFκB) activation on the expression of P-selectin and ICAM1 in acute lung injury (ALI) rats and the effects of low molecular weight heparin (LMWH) and aspirin (ASA) The protective effect and explore its mechanism. Methods Endotoxin was injected into tail vein to prepare ALI rat model. Sixty rats were randomly divided into normal control group, ALI group, LMWH group and ASA group. The expression of NFκB, ICAM1 and P-selectin in lung tissue were observed. Results The activity of NFκB in lung tissue was significantly increased in ALI group. ICAM1 and P-selectin were significantly higher in vascular endothelial cells and bronchial epithelial cells (all P <0.05). The activity of NFκB, ICAM1 and P-selectin in LMWH group and ASA group were decreased, Pathological injury was significantly reduced, ASA treatment group than LMWH group (P all <0.05). Conclusion NFκB activation plays a role in the pathogenesis of ALI. NFκB is involved in the activation of many inflammatory cells such as neutrophils and vascular endothelial cells, and regulates the expression of ICAM1 and P-selectin genes and thus lung injury. LMWH can relieve lung injury by improving microcirculation, indirectly inhibiting NFκB activation, reducing the adhesion of neutrophils and platelets. ASA directly inhibits the activation of NFκB through anti-oxidant properties to reduce lung injury.