Li Xue-Li, Li Kun, Li Yong-Yu, Feng Yan, Gong Qian, Li Yan-Na, Li Xue-Jin, Chen Chang-Jie
Institute of Digestive Disease, Medical School of Tongji University, Shanghai, People's Republic of China.
Cell Stress Chaperones. 2009 Mar;14(2):199-206. doi: 10.1007/s12192-008-0074-9. Epub 2008 Sep 3.
The expression of heat-shock protein 60 (also known as chaperonin 60, Cpn60) in experimental acute pancreatitis (AP) is considered to play an active role in the prevention of abnormal enzyme accumulation and activation in pancreatic acinar cells. However, there are controversial results in the literature regarding the relationship between the abnormality of Cpn60 expression and AP onset and development. The purpose of this study was to investigate the alternations of Cpn60 expression and the relationship between the abnormal expression of Cpn60 and AP progression in rat severe acute pancreatitis (SAP) models. In this report, we induced SAP in Sprague-Dawley (SD) rats by reverse injection of sodium deoxycholate into the pancreatic duct, and examined the dynamic changes of Cpn60 expression in pancreatic tissues from different time points and at different levels with techniques of real-time PCR, western blotting, and immunohistochemistry. At 1 h after SAP induction, the expression of Cpn60 mRNA in the AP pancreatic tissues was higher than those in the sham-operation group and normal control group, but decreased sharply as the time period was extended, and there was a significant difference between 1 h and 10 h after SAP induction (p < 0.05). In the AP process, Cpn60 protein expression showed transient elevation as well, and the increased protein expression occurred predominantly in affected, but not totally destroyed, pancreatic acinar cells. As AP progressed, the pancreatic tissues were seriously damaged, leading to a decreased overall Cpn60 protein expression. Our results show a complex pattern of Cpn60 expression in pancreatic tissues of SAP rats, and the causality between the damage of pancreatic tissues and the decrease of Cpn60 level needs to be investigated further.
热休克蛋白60(也称为伴侣蛋白60,Cpn60)在实验性急性胰腺炎(AP)中的表达被认为在预防胰腺腺泡细胞中异常酶的积累和激活方面发挥着积极作用。然而,关于Cpn60表达异常与AP发病及发展之间的关系,文献中存在有争议的结果。本研究的目的是探讨大鼠重症急性胰腺炎(SAP)模型中Cpn60表达的变化以及Cpn60异常表达与AP进展之间的关系。在本报告中,我们通过向胰管逆行注射脱氧胆酸钠在Sprague-Dawley(SD)大鼠中诱导SAP,并采用实时PCR、蛋白质印迹和免疫组织化学技术检测不同时间点和不同水平胰腺组织中Cpn60表达的动态变化。在诱导SAP后1小时,AP胰腺组织中Cpn60 mRNA的表达高于假手术组和正常对照组,但随着时间的延长急剧下降,且在诱导SAP后1小时和10小时之间存在显著差异(p < 0.05)。在AP过程中,Cpn60蛋白表达也呈现短暂升高,且增加的蛋白表达主要发生在受影响但未完全破坏的胰腺腺泡细胞中。随着AP的进展,胰腺组织严重受损,导致Cpn60蛋白总体表达下降。我们的结果显示了SAP大鼠胰腺组织中Cpn60表达的复杂模式,胰腺组织损伤与Cpn60水平降低之间的因果关系需要进一步研究。