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目的建立大鼠MODS模型,将IκB通过腺病毒载体导入体内,以了解其对MODS大鼠炎性反应的影响。方法50只大鼠随机分为五组:A组(正常对照组),B组(MODS损伤1d组),C组(MODS损伤7d组),D组(腺病毒转载IκB治疗1d组),E组(腺病毒转载IκB治疗7d组)。观察五组大鼠从致伤开始后1、7d的各脏器功能的生化指标,病理组织学及血清TNF-α、IL-6的表达。结果经中心静脉途径导入腺病毒转载的IκB基因,可降低MODS大鼠血肌酐、谷丙转氨酶、总胆红素、肌酸磷酸肌酶水平,改善动脉血氧分压;减轻大鼠病理组织学损伤,降低血液中TNF-α、IL-6含量。结论通过中心静脉途径注入腺病毒转载的IκB基因,直接增加了体内IκB的表达,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最终达到阻断炎症反应的恶性循环,成为治疗MODS新的方向。
OBJECTIVE: To establish a model of MODS in rats and introduce IκB into the body through adenoviral vector to understand its effect on inflammatory reaction in 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 7d with MODS injury), group D (group Ⅰd with adenovirus carrying IκB), group E Group (Adenovirus replication IκB treatment 7d group). The biochemical indexes, histopathology and the expression of serum TNF-α and IL-6 in each group were observed after 1 and 7 days of injury. Results The IκB gene transcribed by adenovirus via central venous route could reduce the levels of serum creatinine, alanine aminotransferase, total bilirubin and creatine phosphokinase in MODS rats, and improve the partial pressure of arterial oxygen and relieve the pathological damage in rats , Lower blood levels of TNF-α, IL-6. Conclusion Intravenous injection of adenovirus carrying IκB gene directly increases the expression of IκB, inhibits the activation of NF-κB and blocks the synthesis of inflammatory cytokines regulated by adenovirus, thus eliminating the massive accumulation of inflammatory cells in the body Eventually reach a vicious circle blocking the inflammatory response, a new direction for the treatment of MODS.