To prepare the effects of rat liver decellularized extracellular matrix scaffold on pancreatic islet cell viability and secretory function, providing a novel biomaterial for pancreatic islet transplantation in type 1 diabetes treatment.

Rat livers were processed using perfusion decellularization. The scaffold structure and core components were characterized through histological staining, immunofluorescence staining, and scanning electron microscopy. The retention of bioactive factors such as platelet-derived growth factor and fibroblast growth factor in the scaffold was detected using ELISA kits. Biocompatibility was assessed via DNA content quantification, DAPI staining, and CCK-8 assay using L929 cells. Functional modification of the decellularized scaffold was achieved by perfusion with platelet-rich plasma (PRP). The effects of the PRP-modified scaffold on pancreatic islet cell viability and function were verified using immunofluorescence staining and cell viability staining. Comparisons between two groups were performed using independent samples t-test, comparisons among three groups were conducted using one-way analysis of variance (ANOVA), followed by LSD-t test for pairwise comparisons. For the two-factor design, a two-way repeated-measures ANOVA was performed, with Bonferroni correction applied for multiple comparisons.

The liver decellularized scaffold prepared by perfusion appeared translucent white macroscopically, retained the natural multi-level vascular structure, and exhibited a porous network morphology microscopically. Various staining methods confirmed significant decellularization efficiency with preservation of core matrix proteins such as type I collagen and fibronectin, as well as multiple bioactive factors. Specifically, the relative retention rates of fibroblast growth factor and glycosaminoglycans reached (88.05 ± 9.87)% and (90.77 ± 3.32)%, respectively. The scaffold demonstrated good biocompatibility, being acellular with residual DNA content as low as (5.25 ± 2.18) ng/mg, and significantly promoted L929 cell proliferation. The scaffold enhanced the insulin secretory function of pancreatic islet cells, the stimulation index in the glucose-stimulated insulin secretion assay for the scaffold group was significantly higher than that of the control group (2.78 ± 0.08 vs 2.33 ± 0.14), with statistical significance (P < 0.01). PRP modification significantly increased the content of growth factors, such as platelet-derived growth factor, in the scaffold, showing statistical significance (P < 0.05). The PRP-modified scaffold positively promoted pancreatic islet cell viability and function.

The preparation process for the rat liver decellularized scaffold is reliable, yielding a scaffold with both structural integrity and bioactivity. The PRP-modified scaffold effectively supports the maintenance of islet cell viability and function, presenting a promising novel scaffold material and technical strategy for islet transplantation.