Genipin-crosslinked decellularized scaffold induces regeneration of defective rat kidneys.

Abstract

Objective: The purpose of this study was to improve the performance of decellularized renal scaffolds by the genipin crosslinking method to facilitate the regeneration of tissues and cells and provide better conditions for the regeneration and repair of defective kidneys. Methods: SD rats were randomly divided into three groups: normal group, uncrosslinked scaffold group and genipin-crosslinked scaffold group. Hematoxylin eosin, Masson and immunofluorescence staining was used to observe the histomorphological characteristics of the kidneys in each group. The preservation of the renal vascular structure in the three groups was observed by vascular casting. A collagenase degradation assay was used to detect the antidegradation ability of the kidney in the three groups. CCK8 assays were used to test the in vitro biocompatibility of the scaffolds. The lower 1/3 of the rat left kidney was excised, and the defect was filled with decellularized renal scaffolds to observe the effect of scaffold implantation on the regenerative ability of the defective kidney. Results: Histological images showed that the genipin-crosslinked scaffold did not destroy the structure of the scaffold, and the collagen fibers in the scaffold was more regular, and the outline of the glomerulus was clearer than uncrosslinked scaffold. The results of casting showed that the vascular structure of genipin-crosslinked scaffold was still intact. The anti-degradation ability test showed that the anti-degradation ability of genipin-crosslinked scaffold was significantly higher than that of the uncrosslinked scaffold. Cell culture experiments showed that the genipin-crosslinked scaffold had no cytotoxicity and promoted cell proliferation to some extent. In vivo scaffold transplantation experiments further demonstrated that the genipin-crosslinked scaffold had better anti-degradation and anti-inflammatory ability. Conclusion: Genipin-crosslinked rat kidney scaffold complemented kidney defects in rats can enhance scaffold-induced kidney regeneration and repair.