Abstract
目的:研究肝硬化大鼠全肝血流阻断后血清中易导致多器官功能损伤的相关炎性因子表达的情况。方法:选用雄性SD大鼠80只,体重160~200 g,30%CCl4油溶液灌胃及饮用5%乙醇水制成肝硬化模型,随机分4组,每组20只。采用阻断肝门、肝上上腔静脉及肝下下腔静脉15 min (A2组)、30 min (A3组)、45 min (A4组)制作肝硬化大鼠全肝血流阻断模型,并以假手术组(A1组)作为对照。按阻断时间活杀取材,采用肝下下腔静脉取血,监测血清中TNF-α、NF-KB及IL-21的表达。多个样本均数比较采用单因素方差分析,两组间比较采用t检验。结果:全肝血流阻断各组与A1组相比血清中TNF-α,NF-KB,IL-21浓度明显升高(P < 0.05),且随时间增加,表达呈逐渐增强趋势。结论:肝硬化大鼠全肝血流阻断后,血清中相关炎性因子的表达浓度是升高的,随阻断时间的延长,因子的浓度呈上升趋势,而不同炎性因子之间存在影响,在器官功能损伤中发挥作用。 Objective: To research the expression of inflammatory cytokines which easily lead to multiple organ damage in liver cirrhosis rats serum under the condition of the whole liver blood flow blocking. Methods: Eights male SD rats weight 160 - 200 g were selected. The liver cirrhosis rats model was established by 30% CCl4 solution to fill the stomach and 5% alcohol to feed. Eighty SD rats were randomly divided into four groups, with 20 rats in each group. By blocking porta hepatis, liver up and inferior vena cava for 15 min (A2 group ), 30 min (A3group), 45 min (A4 group) production of cirrhosis rats whole liver blood flow blocking model, and the sham operation group (A1 group) as control. Twenty rats in each group were sacrificed at 15, 30, 45 min, respectively after modeling. According to the blocking time, they were killed lively, to monitor the expression of TNF-α, NF-KB and IL-21 in the serum from the inferior vena cava. All data were analyzed by using the analysis of variance or t test. Results: Cirrhosis rats whole liver blood flow blocking model compared with those in group A1, levels of TNF-α, NF-KB and IL-21 were significantly increased (p < 0.05), and the expression of inflammatory cytokines trend to grow by time. Conclusion: The expression of inflammatory cytokines which easily lead to multiple organ damage in liver cirrhosis rats serum under the condition of the whole liver blood flow blocking was increased. The concentration of inflammatory cytokines increases with the extension of blocking time. There is a mutual influence among different inflammatory cytokines which play a role in the injury of organ function.
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