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目的:探讨低密度脂蛋白(LDL)在大鼠内毒素血症所致多器官功能障碍综合征(MOSF)中的作用及相关机制。方法:大鼠尾静脉注射脂多糖制作内毒素血症模型。随机分为正常对照组、内毒素血症组和LDL预处理组。每组依时间点再分为1.5h、6h和12h3个亚组。按时间点处死大鼠,留取肺、肠组织及血标本,测定器官功能指标血清天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、尿素氮(BUN)、肌酐(Cr)水平,肺组织髓过氧化物酶(MPO)、小肠组织二胺氧化酶(DAO)活性以及血清细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)浓度。结果:与正常对照组比较,内毒素血症组大鼠血中细胞因子浓度明显增高,TNF-α(P<0.05)、IL-6(P<0.01);器官功能指标中,肺组织MPO活性明显升高(P<0.01);肝脏AST(P<0.01)、ALT(P<0.05)明显升高;肾脏BUN(P<0.05)明显升高;小肠组织DAO(P<0.05)活性显著下降。与内毒素血症组比较,LDL预处理组大鼠血中细胞因子浓度显著降低,TNF-α(P<0.01)、IL-6(P<0.05);肺组织MPO活性明显下降(P<0.05);肝、肾功能指标AST(P<0.01)、ALT(P<0.05)、BUN(P<0.05)明显低于内毒素血症组;小肠组织DAO活性无明显变化(P>0.05)。结论:给予外源性LDL能够结合、失活内毒素,降低血中细胞因子TNF-α、IL-6浓度,从而减轻内毒素血症所致多器官功能障碍。
Objective: To investigate the role and mechanism of low density lipoprotein (LDL) in multiple organ dysfunction syndrome (MOSF) induced by endotoxemia in rats. Methods: Rats were injected lipopolysaccharide into the tail vein to make the model of endotoxemia. Randomly divided into normal control group, endotoxemia group and LDL pretreatment group. Each group according to the time point is divided into 1.5h, 6h and 12h3 subgroups. The rats were sacrificed at time points, and the lung, intestine tissue and blood samples were collected for determination of organ function indexes such as serum AST, ALT, BUN and creatinine , Myeloperoxidase (MPO) and diamine oxidase (DAO) activity in the lung tissue, as well as the levels of serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL- Results: Compared with the normal control group, the concentrations of cytokines in the blood of the endotoxemia group were significantly increased, the levels of TNF-α (P <0.05), IL-6 (P <0.01) (P <0.01). The liver AST (P <0.01) and ALT (P <0.05) increased significantly. The renal BUN (P <0.05) increased significantly. The activity of DAO (P <0.05) decreased significantly in the small intestine. Compared with the endotoxemia group, the concentrations of cytokines in the LDL preconditioning group were significantly decreased (P <0.01), IL-6 (P <0.05), and the MPO activity in the lung tissue was significantly decreased (P <0.05 (P <0.01), ALT (P <0.05), and BUN (P <0.05) in endotoxemia group. There was no significant change in DAO activity in small intestine (P> 0.05). Conclusion: Exogenous LDL can be combined to inactivate endotoxin and reduce the levels of TNF-α and IL-6 in blood, so as to relieve the multiple organ dysfunction caused by endotoxemia.