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目的:观察过氧化物酶增殖物激活受体γ(PPARγ)及其激动剂罗格列酮注对多器官功能障碍综合征(MODS)大鼠炎性反应的影响。方法:50只大鼠随机分为5组:A组(正常对照组),B组(MODS损伤1d组),C组(MODS损伤3d组),D组(PPARγ激动剂预处理1d组),E组(PPARγ激动剂预处理3d组)。观察5组大鼠从致伤开始后1、3d的各脏器功能的生化指标,病理组织学,大鼠外周血单个核细胞内转录因子PPARγ、NF-κBp65的表达及血清TNF-α、IL-6的表达。结果:经股静脉途径注入PPARγ激动剂罗格列酮可降低MODS大鼠总胆红素(TB)、谷丙转氨酶(ALT)、谷草转氨酶(AST)水平;减轻大鼠病理组织学损伤,降低血液中TNF-α、IL-6的水平。结论:通过股静脉途径注入PPARγ激动剂,抑制了NF-κB的活化,阻断其所调控的炎症因子的合成,从而消除炎性细胞在体内的大量聚集,阻断炎症反应的恶性循环,成为治疗MODS新的方向。
Objective: To observe the effects of peroxisome proliferator - activated receptor γ (PPARγ) and its agonist rosiglitazone on the inflammatory response in multiple organ dysfunction syndrome (MODS) rats. Methods: Fifty rats were randomly divided into five groups: group A (normal control group), group B (group 1d with MODS injury), group C (group 3d with MODS injury), group D (group with PPARγ agonist pretreatment for 1d) Group E (PPARγ agonist pretreatment 3d group). The biochemical indexes, pathological histology, the expression of PPARγ, NF-κBp65 in rat peripheral blood mononuclear cells and the levels of serum TNF-α, IL -6 expression. Results: Rosiglitazone, a PPARγ agonist, was injected into femoral vein to reduce the levels of total bilirubin (TB), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in rats with MODS. Blood levels of TNF-α, IL-6. CONCLUSION: Injecting PPARγ agonist through the femoral vein can inhibit the activation of NF-κB and block the synthesis of inflammatory cytokines regulated thereby, which can eliminate the massive accumulation of inflammatory cells in the body and block the vicious cycle of inflammatory reaction, becoming Treatment of MODS new direction.