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目的 探讨山莨菪碱 ( 65 4-2 )对多器官功能障碍综合征 (MODS)可能的治疗机制。方法 采用失血性休克合并内毒素刺激诱发MODS家兔模型 ,2 4只大耳白兔随机分为正常对照组 (C组 )、模型组 (M组 )、65 4-2治疗组 (T组 )。用原位杂交 (ISN)技术、凝胶电泳迁移率改变 (EMSA)及酶联免疫吸附试验 (ELISA)法分别检测肺泡巨噬细胞 (PAM )及肝枯否细胞 (KC)中I -кB激酶(IKK -β)mRNA表达、NF -кB的活性和细胞培养上清液中TNF -α的含量。并进行动脉血气、生化和内脏组织病理学光镜检查。 结果 M组和C组比较PAM和KC中IKK -βmRNA表达 [( 0 15± 0 0 3 ) ;( 0 17± 0 0 4) ] ,NF -кB活性 [( 1 49± 0 3 0 ) ;( 1 72± 0 3 6) ]和上清液TNF -α的含量 [( 2 79 74± 2 5 91) ;( 3 0 0 0 5± 3 0 86)ng/L]明显增高 ( P 均 <0 0 1)。肝肺肾小肠等脏器功能发生不同程度损害 ;65 4-2治疗组能显著抑制M组PAM和KC中IKK -βmRNA表达 [( 0 10± 0 0 2 ) ;( 0 11± 0 0 2 ) ]、NF -кB活性 [( 0 65±0 10 ) ;( 0 88± 0 2 0 ) ]和TNF -α[( 180 61± 13 0 1) ;( 2 10 2 8± 18 0 1)ng/L]的分泌 (P <0 0 1或P <0 0 5 )。明显缓解MODS动物内脏组织的功能损害。结论 65 4-2通过抑制IKK -β/NF -κB
Objective To investigate the possible therapeutic mechanism of anisodamine (65 4-2) on multiple organ dysfunction syndrome (MODS). Methods 24 rabbits were randomly divided into normal control group (C group), model group (M group) and 654-2 treatment group (T group) . In situ hybridization (ISN), electrophoretic mobility shift assay (EMSA) and enzyme linked immunosorbent assay (ELISA) were used to detect I-kappaB kinase in alveolar macrophages (PAM) (IKK-β) mRNA expression, NF-κB activity and TNF-α content in cell culture supernatant. And arterial blood gas, biochemical and visceral histopathology light microscopy. Results The expression of IKK-βmRNA in PAM and KC was significantly higher in M group and C group than that in C group [(0 15 ± 0 0 3); (0 17 ± 0 0 4)], NF-κB activity [(1 49 ± 0 3 0) 1 72 ± 0 3 6)], and the level of TNF-α in the supernatant [(2 79 74 ± 2 5 91); (300 0 ± 3 0 86) ng / L] 0 1). The function of liver, lung, kidney, small intestine and other organs were damaged to some extent. 65 4-2 treatment group could significantly inhibit the expression of IKK-βmRNA in PAMs and KCs in M group [(0 10 ± 0 0 2); (0 11 ± 0 0 2) ], NF-κB activity [(0 65 ± 0 10); (0 88 ± 0 2 0)] and TNF-α [(180 61 ± 13 0 1); (2 10 2 8 ± 18 0 1) L] secretion (P <0.01 or P <0 05). Significantly alleviate the functional impairment of MODS animal visceral tissue. Conclusion 65 4-2 inhibits IKK-β / NF-κB