八肽胆囊收缩素对脂多糖诱导大鼠肺组织NF-κB活性增高的抑制作用

Inhibitory effect of cholecystokinin octapeptide on NF-κB activity induced by lipopolysaccharide in rat lungs

目的与方法 :为探讨八肽胆囊收缩素 (CCK - 8)防治内毒素引起急性肺损伤的分子作用机理 ,用电泳迁移率变动分析技术 (EMSA) ,观察CCK - 8对脂多糖 (LPS)诱导核转录因子κB(NF -κB)活性变化的影响 ,用光密度扫描电泳谱带峰面积积分值表示NF -κB活性 ,观察肺组织的病理学变化。结果 :LPS入血可以明显引起大鼠肺组织的NF -κB活性 16 39 92± 198 6 3(P <0 0 1) ,显著高于对照组 (5 93 5 6± 89 34) ,此作用为预先静脉注入CCK - 8部分逆转 ,NF -κB活性低至 82 3 91± 97 32 (P <0 0 1) ,CCK - 8可减轻LPS引起的肺组织病理学变化。结论 :CCK -8对LPS激活肺组织NF

AIM and METHODS: To investigate molecular mechanism of cholecystokinin octapeptide(CCK-8) protection aganist acute lung injury induced by lipopolysaccharide (LPS),effect of CCK-8 on nuclear transcription factor-kappa B(NF-κB) activity in rat lungs was measured with electrophoretic mobility shift assay(EMSA) during endotoxemia. NF-κB activity was expressed as peak areas integration of electrophoresis bands. The effect of CCK-8 on lung injury induced by LPS was observed. RESULTS: The administration of LPS to blood induced significant increase in NF-κB activity from 593 56±89 34 of control to 1 639 92±198 63( P< 0 01),which was in part reversed by pretreatment of CCK-8 (823 91±97 32, P< 0 01). Compared to the control, the CCK-8 pretreatment group also showed the lighter lung injury by pathological examination. CONCLUSION: CCK-8 had the inhibitory effect on NF-κB activity induced by LPS.