早期生长反应因子-1和组织因子在大鼠胰腺炎组织中的表达

Expressions of early growth response 1 and tissue factor in caerulein-induced acute pancreatitis tissues in rats

目的观察早期生长反应因子-1(Egr-1)和组织因子(TF)在实验性大鼠急性胰腺炎组织中的表达。方法以大剂量雨蛙素(每小时腹腔注射20 μg/kg·b.w.,连续4 h)诱导建立大鼠急性实验性胰腺炎模型。观察刺激后30 min至4 h时急性胰腺炎组织Egr-1 mRNA和蛋白的表达以及TF mRNA的表达,并进行免疫组织化学检测。结果大剂量雨蛙素刺激后,大鼠胰腺呈典型的胰腺炎改变。刺激后30 min胰腺组织Egr-1 mRNA表达达到高峰,然后逐渐下降。但Egr-1蛋白水平在刺激后2 h达到高峰。组织学观察发现,刺激后2 h,几乎每个胰腺腺泡细胞均表达Egr-1蛋白,并大多集中在细胞核。TF mRNA的表达在刺激后1 h出现,并在4 h内逐渐增高。大剂量的蛙皮素刺激胰腺组织仅引起少量的Egr-1 mRNA的表达。结论Egr-1作为一种前炎性转录因子在急性胰腺炎的发生中可能起着重要的作用,这一作用在一定程度上可能是通过调节TF的表达而实现的。

s: Objective To observe the expressions of early growth response 1 (Egr-1) and tissue factor (TF) in rat tissues of acute pancreatitis induced by caerulein and to explore their significance. Methods Pancreatitis was induced in rats by high-dose intraabdominal caerulein injection. The changes of Egr-1 mRNA and protein in pancreas were measured by quantitative PCR and Western blotting, and the localization of Egr-1 protein in acinar cells was visualized by immunohistochemistry. TF mRNA levels were also measured by quantitative PCR. High-dose bombesin-stimulated rats served as the negative control. Results Egr-1 mRNA was rapidly increased in the pancreas of rats stimulated by high-dose cearulein, and reached the peak level 30 min after the stimulation, whereas band for peak Egr-1 protein level was visualized by Western blotting till 2 h after stimulation. Immunohistochemistry showed that almost every acinar cell in the pancreas was Egr-1-positive, especially in the nucleus. In line with Egr-1 activation, TF mRNA was detected 1 h after the stimulation and increased steadily within the initial 4 h. Only a small quantity of Egr-1 mRNA expression was observed in bombesin-stimulated rats, in which no Egr-1 protein or TF mRNA were detected. Conclusion Egr-1 mRNA and protein were up-regulated in the early stage of pancreatitis. Egr-1, as a pro-inflammatory transcriptional factor, probably plays an important role in the initiation of acute pancreatitis, and its action might be partially mediated through the up-regulation of TF expression.