Warzecha Z, Dembinski A, Ceranowicz P, Konturek S J, Tomaszewska R, Stachura J, Konturek P C
Department of Physiology, Jagiellonian University Medical School, Kraków, Poland.
J Physiol Pharmacol. 2003 Dec;54(4):575-90.
BACKGROUND/AIM: Insulin-like growth factor-1 (IGF-1) and other growth factors overexpression was reported in acute pancreatitis. Previous studies have shown the protective effect of epidermal growth factor (EGF), Hepatocyte Growth Factor (HGF) and Fibroblast Growth Factor (FGF) in the course of experimental acute pancreatitis. The aim of our studies was to determine the effect of IGF-1 administration on the development of caerulein-induced pancreatitis.
Acute pancreatitis was induced by infusion of caerulein (10 micro/kg/h) for 5 h. IGF-1 was administrated twice at the doses: 2, 10, 50, or 100 micro/kg s.c.
Administration of IGF-1 without induction of pancreatitis increased plasma interleukin-10 (IL-10). Infusion of caerulein led to development of acute edematous pancreatitis. Histological examination showed pancreatic edema, leukocyte infiltration and vacuolization of acinar cells. Also, acute pancreatitis led to an increase in plasma lipase and interleukin 1beta (IL-1beta) level, whereas pancreatic DNA synthesis and pancreatic blood flow were decreased. Treatment with IGF-1, during induction of pancreatitis, increased plasma IL-10 and attenuated the pancreatic damage, what was manifested by histological improvement of pancreatic integrity, the partial reversion of the drop in pancreatic DNA synthesis and pancreatic blood flow, and the reduction in pancreatitis-evoked increase in plasma amylase, lipase and IL-1beta level. Protective effect of IGF-1 administration was dose-dependent. Similar strong protective effect was observed after IGF-1 at the dose 2 x 50 and 2 x 100 microg/kg.
(1) Administration of IGF-1 attenuates pancreatic damage in caerulein-induced pancreatitis; (2) This effect is related, at least in part, to the increase in IL-10 production, the reduction in liberation of IL-1beta and the improvement of pancreatic blood flow.
背景/目的：据报道，胰岛素样生长因子-1（IGF-1）及其他生长因子在急性胰腺炎中呈过表达。既往研究已表明表皮生长因子（EGF）、肝细胞生长因子（HGF）和成纤维细胞生长因子（FGF）在实验性急性胰腺炎病程中具有保护作用。我们研究的目的是确定给予IGF-1对雨蛙肽诱导的胰腺炎发展的影响。
通过输注雨蛙肽（10微克/千克/小时）5小时诱导急性胰腺炎。以2、10、50或100微克/千克的剂量皮下注射IGF-1两次。
在未诱导胰腺炎的情况下给予IGF-1可使血浆白细胞介素-10（IL-10）升高。输注雨蛙肽导致急性水肿性胰腺炎的发生。组织学检查显示胰腺水肿、白细胞浸润及腺泡细胞空泡化。此外，急性胰腺炎导致血浆脂肪酶和白细胞介素1β（IL-1β）水平升高，而胰腺DNA合成及胰腺血流减少。在诱导胰腺炎期间用IGF-1治疗可使血浆IL-10升高，并减轻胰腺损伤，表现为胰腺完整性的组织学改善、胰腺DNA合成及胰腺血流下降的部分逆转，以及胰腺炎诱发的血浆淀粉酶、脂肪酶和IL-1β水平升高的降低。给予IGF-1的保护作用呈剂量依赖性。在给予2×50和2×100微克/千克剂量的IGF-1后观察到类似的强大保护作用。
（1）给予IGF-1可减轻雨蛙肽诱导的胰腺炎中的胰腺损伤；（2）这种作用至少部分与IL-10产生增加、IL-1β释放减少及胰腺血流改善有关。
