摘要目的 检测急性坏死性胰腺炎(severe acute pancreatitis,ANP)大鼠肺组织巨噬细胞移动抑制因子(MIF)mRAN表达及TNF-α含量,探讨它们在ANP肺损伤中的作用机制.方法 40只SD大鼠随机分成对照组及ANP 3、6、12 h组.采用5%牛磺胆酸钠(0.1 ml/100 g体重)胆胰管逆行注射方法制备ANP模型.取血检测血清淀粉酶.取胰腺组织和肺组织行病理学检查,并称重计算其湿/干重比.采用RT-PCR法检测肺组织MIF mRNA表达,放免法测定肺组织TNF-α含量.结果 ANP组血淀粉酶、胰腺和肺组织湿/干重比显著升高,病理损伤随时间延长逐渐加重.ANP 3、6、12 h组肺组织TNF-α含量分别为(0.69±0.07)ng/ml、(1.64±0.10)ng/ml和(0.92±0.11)ng/ml;MIF mRNA表达量分别为1.97±0.09、2.55±0.23、3.29±0.26,均显著高于对照组的(0.19±0.06)ng/ml和1.21±0.34(P值均<0.01).肺组织MIFmRNA表达与肺组织病理损伤、肺湿干重比、TNF-α含量均呈正相关,相关系数分别为r=0.637、r=0.684、r=0.858,P值均<0.01.肺组织TNF-α含量与肺损伤、肺湿/干重比均呈正相关,相关系数分别为r=0.540和r=0.421,P值均<0.01.结论 ANP大鼠肺组织MIFmRNA过表达,TNF-α含量显著增加,它们共同参与肺损伤的发生.

abstractsObjective To investigate the relationship between the expression of MIF mRNA and TNF-α in the lung tissue of rats with acute necrotizing pancreatitis (ANP) and explore their mechanism of action in acute lung injury during the course of ANP. Methods A total of 40 Sprague-Dawley rats were randomly divided into four groups (n = 10 in each group) : the sham operation (SO) group, ANP 3h group, 6h group, 12h group. The model of ANP was induced by retrograde injection of 5% sodium tanrocholate (0. 1 ml/100 g) into the biliary and pancreatic duct. The level of serum amylase was determined;pancreatic and lung tissues were harvested for pathological examination, and wet/dry weight ratios were estimated. Intrapulmonary expression of MIF mRNA was assayed by semi-quantitative RT-PCR. TNF-α in pulmonary homogenate was measured by immunoradiometric assay. Results Serum amylase, wet/dry weight ratios of pancreatic and lung tissues all significantly increased, and pathological injuries aggravated with time in ANP groups. Levels of TNF-α in ANP 3h, 6h, 12h group were (0.69 ± 0. 107) ng/ml, (1.64 ± 0. 10) ng/ml and (0.92 ± 0.11) ng/ml, and expression of MIF mRNA were 1.97±0.09, 2.55±0.23, 3.29±0.26, which were significantly higher than those in control group [(0. 19±0.06)ng/ml, 1.21±0.34, P<0.01]. lntrapulmonary expression of MIF mRNA was positively associated with lung pathological injuries, wet/dry weight ratio, and TNF-α(r = 0. 637, r = 0.684, r = 0.858, P < 0.01). Intrapulmonary levels of TNF-α was positively associated with lung pathological injuries, wet/dry weight ratio (r=0.540, r=0.421, P<0.01). Conclusions MIF mRNA was over- expressed and level of TNF-α was significantly increased in pulmonary tissue in rats with ANP, and this may be one of the mechanisms in the pathogenesis of lung injury in ANP.