Role of Wnt/β-catenin pathway agonist SKL2001 in Caerulein-induced acute pancreatitis
The goal of this study was to clarify the protective role of the Wnt/β-catenin pathway agonist SKL2001 in a rat model of Caerulein-induced acute pancreatitis. AR42J cells and rats were divided into 4 groups: control, Caerulein, SKL2001 + Caerulein, and SKL2001 + control. Cell apoptosis
was examined using flow cytometry. Hematoxylin–eosin staining was performed to observe pathological changes in pancreatic and small intestinal tissues. Inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA), while genes related to the Wnt/β-catenin pathway
were quantified using quantitative real-time PCR. In vitro results showed that Caerulein promoted cell necrosis, inhibited the Wnt/β-catenin pathway, and increased the level of inflammatory cytokines. However, SKL2001 reduced cell necrosis and inflammatory cytokines and activated the
Wnt/β-catenin pathway. Additionally, in vivo results demonstrated the accumulation of fluid (i.e., edema), hemorrhage, inflammation and necrosis of the pancreatic acini occurred 6 h after the final Caerulein induction, with the damage reaching a maximal level 12 h after the final Caerulein
induction; meanwhile, the Wnt/β-catenin pathway was evidently inhibited with an enhanced level of inflammatory cytokines. The aforementioned damage was further aggravated 12 h later. Nevertheless, the pancreatic and small intestinal tissue damages were alleviated in Caerulein-induced
rats treated with SKL2001. In conclusion, activation of the Wnt/β-catenin pathway could inhibit Caerulein-induced cell apoptosis and inflammatory cytokine release, thus improving pancreatic and intestinal damage in rats with acute pancreatitis.
Keywords: AR42J cells; Caerulein; SKL2001; Wnt/β-catenin pathway; acute pancreatitis; cellules AR42J; cæruléine; pancréatite aiguë; voie de signalisation Wnt/β-caténine
Document Type: Research Article
Affiliations: 1: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China. 2: Department of Gastroenterology, The Second Affiliated Hospital of Guangxi Medical University, Nanning 530007, Guangxi Zhuang Autonomous Region, China. 3: Department of Clinical Laboratory, The First People’s Hospital of Jingzhou City, Jingzhou, Jingzhou 434000, Hubei, China.
Publication date: 01 January 2019
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