【摘要】 目的探讨核因子-κB(NF-κB)激活及细胞凋亡在大鼠重症急性胰腺炎(SAP)肺组织损伤中的作用。方法 SD大鼠随机分为对照组、SAP组、PDTC预处理组。建立各组模型后取肺组织行光镜下病理观察,免疫组织化学法观察NF-κB的表达,TUNEL法观察细胞凋亡情况。结果对照组细胞结构基本正常,仅极少量NF-κB活化,且只有少量肺泡间质细胞和肺泡上皮细胞凋亡。SAP组中NF-κB表达及细胞凋亡指数均明显升高,并呈动态变化,6 h达高峰,NF-κB表达及凋亡细胞主要见于中性粒细胞、单核/巨噬细胞、支气管黏膜上皮细胞、肺泡上皮细胞。PDTC预处理组病理改变减轻,NF-κB表达及细胞凋亡指数均明显下降,但仍高于对照组。结论 SAP时肺组织NF-κB活化并通过诱导细胞凋亡参与肺损伤。PDTC可能通过抑制NF-κB活性及细胞凋亡减轻重症急性胰腺炎并发肺损伤。更多还原

【Abstract】 【Objective】To explore the relationship between intrapulmonary activition of nuclear factor-κB(NFκB),cell apoptosis and pulmonary injury in rats with severe acute pancreatitis(SAP).【Methods】112 SD rats were randomly divided into control group,SAP group and PDTC pretreated group,and each or the above groups were respectively divided into 4 subgroups at different time points after operation(3 h,6 h,9 h,12 h).SAP was induced by retrograde injection of 5% sodium taurocholate into the bile-pancreatic duct(0.1 mL/100 g).Histological changes of lungs were observed after hematoxylin-eosin(HE) staining.Activation of NF-κB in pulmonary tissues was detected by immunohistochemical method.Cell apoptosis in pulmonary tissues was observed by TUNEL method.【Results】 Only a little positive signals were observed and a small number of apoptosis cell was seen in epithelial and interstitial cells of lung alveolar in the control group.The expression of NF-κB and apoptosis index significantly increased and exhibited a consectutive changes,reached its peak at 6h.The positive signals and apoptotic cells were mostly observed in neutrophils,macrophages,bronchial epithelial cells and alveoloar epthelial cells.The PDTC pretreated groups showed pathological changes decreased.The expression level of NF-κB and apoptosis index was significantly weaker than that in SAP groups,but still significantly higher than that in control groups(P <0.05).【Conclusions】The activation of NF-κB and then inducing apoptosis may be involved in the SAP lung injury.PDTC might inhibit the activation of NF-κB and apoptosis and then effectively alleviate severity of lung injury.更多还原