论文部分内容阅读
目的探讨NF-κB诱骗寡脱氧核苷酸对大鼠内毒素性肝损伤的保护作用及其机制。方法60只SD大鼠随机分为对照组、内毒素(LPS)组、诱骗寡核苷酸(decoy ODNs)处理组。取各组大鼠肝组织检测NF-κB蛋白结合活性(EMSA),观察组织病理学改变(光镜)及肝细胞凋亡(TUNEL)。取静脉血检测AST(自动生化仪)以及TNF-α,IL-6的表达水平(ELISA)。结果与对照组相比,内毒素组NF-κB活性明显升高,诱发大量肝细胞凋亡,肝脏损伤明显;同时血清AST,TNF-α及IL-6明显升高(P<0.01)。与内毒素组相比,NF-κB诱骗寡核苷酸处理组NF-κB活性受抑制(P<0.01)、肝脏组织病理学改变和肝细胞凋亡明显减轻,血清中TNF-α和AST表达水平降低(P<0.01),但IL-6表达与内毒素组差异无统计学意义(P>0.05)。结论NF-κB诱骗策略能高效抑制NF-κB的活性,抑制其下游有害细胞因子的产生,从而减轻内毒素性肝损伤。
Objective To investigate the protective effect of NF-κB decoy oligodeoxynucleotides on endotoxin-induced liver injury in rats and its mechanism. Methods Sixty SD rats were randomly divided into control group, LPS group and decoy ODNs group. The liver tissues of rats in each group were tested for NF-κB binding activity (EMSA), histopathological changes (light microscope) and hepatocyte apoptosis (TUNEL) were observed. Venous blood samples were taken for AST (automatic biochemical analyzer) and TNF-α and IL-6 expression levels (ELISA). Results Compared with the control group, the activity of NF-κB in endotoxin group was significantly increased, which induced a large number of hepatocyte apoptosis and obvious hepatic injury. At the same time, the levels of serum AST, TNF-α and IL-6 were significantly increased (P <0.01). Compared with the endotoxin group, the NF-κB decoy oligodeoxynucleotide inhibited NF-κB activity (P <0.01), liver histopathological changes and hepatocyte apoptosis were significantly reduced, and the levels of TNF-α and AST in serum (P <0.01), but there was no significant difference between IL-6 expression and endotoxin group (P> 0.05). Conclusion NF-κB decoy strategy can effectively inhibit the activity of NF-κB, inhibit the production of harmful cytokines downstream, thereby reducing endotoxin-induced liver injury.