【摘要】 目的观察核因子-κB(NF-κB)在重症急性胰腺炎(SAP)大鼠胰、肺组织内的表达及肺组织内细胞凋亡情况。方法 SD大鼠60只,分为对照组、SAP组、二硫代氨基甲酸吡咯烷(pyrrolidine dithiocarbamate,PDTC)预处理组。5%牛磺胆酸钠胰胆管逆行注射诱发大鼠SAP模型。SP法观察NF-κB在胰、肺组织内的表达情况,TUNEL法检测肺组织内细胞凋亡情况。结果 SAP组各时间点NF-κB在胰、肺组织内的阳性表达水平与对照组相比均明显增加(P<0.01),PDTC预处理组各时间点NF-κB阳性表达水平与SAP组相比均明显减弱(P<0.05)。SAP组肺组织内凋亡指数高于相对应的对照组(P<0.05),PDTC预处理组凋亡指数均低于相对应的SAP组(P<0.05)。结论 NF-κB的激活和凋亡细胞的增多是加重肺损伤的重要因素之一。PDTC对SAP肺损伤的保护作用可能与抑制NF-κB激活及肺组织内细胞凋亡相关。更多还原

【Abstract】 Objective To investigate the effect of pyrrolidine dithiocarbamate(PDTC) on NF-κB expression and apoptosis in severe acute pancreatitis(SAP)-associated lung injury in rat. Methods 60 SD rats were randomized into control group, SAP group and PDTC pretreated group. SAP model was induced by retrogradely injection of 5% sodium taurocholate into the bile-pancreatic duct. Activation of NF-κB in pulmonary tissues and pancreas tissues was detected by Streptavifin/Peroxidase methods. Intrapulmonary cell apoptosis was detected with TdT-mediated dUTP nick end labeling(TUNEL). Results The expression levels of NF-κB in lung and pancreatic tissues were higher in SAP group than in control group(P <0.01), lower in all PDTC pretreated groups than in SAP groups(P <0.05). The apoptosis index in lung tissue was higher in SAP group than in control group( P<0.05), lower in all PDTC pretreated groups than in SAP groups(P < 0.05). Conclusion NF-κB activation and the increased number of apoptotical cells may be involved in inducing pulmonary microvascular endothelial cell injury, caused thereby circulatory disturbance and aggravated lung injury. Protective effect of PDTC pretreatment on the SAP-associated lung injury may be related to the inhibition of NF-κB activation and apoptosis in lung tissue.更多还原