Purpose: Peroxisome proliferator-activated receptor gamma (PPAR-γ) has a key role in hepatic fibrogenesis by virtue of its effect on the hepatic stellate cells (HSCs). Although many studies have shown that PPAR-γ agonists inhibit liver fibrosis, the mechanism remains largely unclear, especially regarding the cross-talk between PPAR-γ and other potent fibrogenic factors. Methods: This experimental study involved 25 male Wistar rats. Twenty rats were subjected to bile duct ligation (BDL) to induce liver fibrosis, further divided into an untreated group (BDL; n=10) and a group treated with the PPAR-γ agonist thiazolidinedione (TZD), at 14 days post-operation (BDL+TZD; n=10). The remaining 5 rats had a sham operation (sham; n=5). The effect of PPAR-γ agonist on liver fibrosis was evaluated by histopathology, protein immunohistochemistry, and mRNA expression quantitative polymerase chain reaction. Results: Histology and immunostaining showed markedly reduced collagen deposition, bile duct proliferation, and HSCs in the BDL+TZD group compared to those in the BDL group (p<0.001). Similarly, significantly lower mRNA expression of collagen α-1(I), matrix metalloproteinase-2, platelet-derived growth factor (PDGF)-B chain, and connective tissue growth factor (CTGF) were evident in the BDL+TZD group compared to those in the BDL group (p=0.0002, p<0.035, p<0.0001, and p=0.0123 respectively). Moreover, expression of the transforming growth factor beta1 (TGF-β1) was also downregulated in the BDL+TZD group (p=0.0087). Conclusion The PPAR-γ agonist inhibits HSC activation in vivo and attenuates liver fibrosis through several fibrogenic pathways. Potent fibrogenic factors such as PDGF, CTGF, and TGF-β1 were downregulated by the PPAR-γ agonist. Targeting PPAR-γ activity may be a potential strategy to control liver fibrosis.

An 18-year-old woman with annular pancreas and duodenal duplication presented with recurrent acute pancreatitis and underwent a resection of duodenal duplication. However, the patient experienced recurrent abdominal pain after resection. Abdominal computed tomography and magnetic resonance imaging showed a dilatation of the peripheral pancreatic duct and stenosis and malformation of both the Wirsung's and Santorini's duct due to multiple stones. The modified puestow procedure was performed. The main pancreatic ducts in the body and tail were opened, and the intrapancreatic common bile duct was preserved. A Roux-en-Y pancreatico-jejunostomy was performed for reconstructing the pancreaticobiliary system after removing the ductal protein plug. The patient experienced no abdominal pain, no significant elevation of the serum amylase and lipase levels, and no stone formation during the 2 years of follow-up. This procedure is considered to be beneficial for pediatric patients with chronic pancreatitis due to annular pancreas and duodenal duplication.