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Pancreatic disorders such as pancreatitis, pancreatic cancer, cystic fibrosis, and diabetes mellitus can lead to severe destruction of the pancreatic parenchyma, resulting in secondary conditions that compromise patient health. Study models have been developed to better understand the pancreatic regeneration process, which is crucial for advancing therapeutic strategies. These models are particularly relevant for exploring how pancreatic cells can regenerate and proliferate from pre-existing ones. However, the impact of the inflammation caused by biological or synthetic scaffolds used in these studies has not yet been fully evaluated. In this study, we used a synthetic polyether-polyurethane matrix to induce the proliferation of pancreatic parenchyma in vivo in diabetic C57BL/6 mice. After chemical induction of diabetes using streptozotocin (STZ), the animals were divided into two groups, with only one group (G2) receiving daily subcutaneous insulin treatment to assess the influence of glycemia on pancreatic proliferation and inflammation. Two groups (G1 and G2) received synthetic matrices surgically placed adjacent to the native pancreas, which were, and removed 30 days after implantation. Pancreatic proliferation, blood vessel formation inflammatory markers were then analyzed in the matrix. The analyses revealed that the insulin-treated group had a larger intra-implant proliferation area. Examination of angiogenesis in the intra-implant pancreatic tissue through histology and immunobiochemical methods showed an increase in the number of vessels but a decrease in VEGF levels. Furthermore, an increase in all inflammatory markers was observed in the insulin-treated group. The study demonstrated that inflammatory markers may play a significant role in the proliferation, migration, and transdifferentiation of pancreatic cells within the synthetic polyether-polyurethane matrix model, with better outcomes observed when the animals were in normoglycemic conditions.
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