Bluth Martin H, Patel Sameer A, Dieckgraefe Brian K, Okamoto Hiroshi, Zenilman Michael E
Department of Surgery, State University of New York-Downstate Medical Center, Brooklyn, New York, USA.
World J Gastroenterol. 2006 Jul 28;12(28):4511-6. doi: 10.3748/wjg.v12.i28.4511.
Pancreatic regenerating protein (reg I) stimulates pancreatic regeneration after pancreatectomy and is mitogenic to ductal and beta-cells. This suggests that reg I and its receptor may play a role in recovery after pancreatic injury. We hypothesized that reg I and its receptor are induced in acute pancreatitis.
Acute pancreatitis was induced in male Wistar rats by retrograde injection of 3% sodium taurocholate into the pancreatic duct. Pancreata and serum were collected 12, 24, and 36 h after injection and from normal controls (4 rats/group). Reg I receptor mRNA, serum reg I protein, and tissue reg I protein levels were determined by Northern analysis, enzyme-linked immunosorbent assay (ELISA), and Western analysis, respectively. Immunohistochemistry was used to localize changes in reg I and its receptor.
Serum amylase levels and histology confirmed necrotizing pancreatitis in taurocholate treated rats. There was no statistically significant change in serum reg I concentrations from controls. However, Western blot demonstrated increased tissue levels of reg I at 24 and 36 h. This increase was localized primarily to the acinar cells and the ductal cells by immunohistochemistry. Northern blot demonstrated a significant increase in reg I receptor mRNA expression with pancreatitis. Immunohistochemistry localized this increase to the ductal cells, islets, and acinar cells.
Acute pancreatitis results in increased tissue reg I protein levels localized to the acinar and ductal cells, and a parallel threefold induction of reg I receptor in the ductal cells, islets, and acinar cells. These changes suggest that induction of reg I and its receptor may be important for recovery from acute pancreatitis.
胰腺再生蛋白（reg I）可刺激胰腺切除术后的胰腺再生，并且对导管细胞和β细胞具有促有丝分裂作用。这表明reg I及其受体可能在胰腺损伤后的恢复过程中发挥作用。我们推测reg I及其受体在急性胰腺炎中会被诱导表达。
通过向雄性Wistar大鼠的胰管逆行注射3%牛磺胆酸钠诱导急性胰腺炎。在注射后12、24和36小时以及从正常对照组（每组4只大鼠）采集胰腺和血清。分别通过Northern印迹分析、酶联免疫吸附测定（ELISA）和Western印迹分析来测定Reg I受体mRNA、血清reg I蛋白和组织reg I蛋白水平。采用免疫组织化学方法定位reg I及其受体的变化。
血清淀粉酶水平和组织学检查证实牛磺胆酸钠处理的大鼠发生了坏死性胰腺炎。与对照组相比，血清reg I浓度没有统计学上的显著变化。然而，Western印迹显示在24和36小时时组织中reg I水平升高。通过免疫组织化学，这种升高主要定位于腺泡细胞和导管细胞。Northern印迹显示胰腺炎时reg I受体mRNA表达显著增加。免疫组织化学将这种增加定位于导管细胞、胰岛和腺泡细胞。
急性胰腺炎导致腺泡和导管细胞中组织reg I蛋白水平升高，并且导管细胞、胰岛和腺泡细胞中reg I受体平行地诱导增加三倍。这些变化表明reg I及其受体的诱导可能对急性胰腺炎的恢复很重要。
