RESUMEN
Hydrogel microfibers are hydrogel materials engineered into fiber structures. Techniques such as wet spinning, microfluidic spinning, and 3D bioprinting are often used to prepare microfibers due to their ability to precisely control the size, morphology, and structure of the microfibers. Microfibers with different structural morphologies have different functions; they provide a flow-through culture environment for cells to improve viability, and can also be used to induce the differentiation of cells such as skeletal muscle and cardiac muscle cells to eventually form functional organs in vitro through special morphologies. This Review introduces recent advances in microfluidics, 3D bioprinting, and wet spinning in the preparation of microfibers, focusing on the materials and fabrication methods. The applications of microfibers in tissue engineering are highlighted by summarizing their contributions in engineering biomimetic blood vessels, vascularized tissues, bone, heart, pancreas, kidney, liver, and fat. Furthermore, applications of engineered fibers in tissue repair and drug screening are also discussed.
Asunto(s)
Materiales Biocompatibles , Ingeniería de Tejidos , Humanos , Materiales Biocompatibles/química , Materiales Biocompatibles/farmacología , Hidrogeles/química , Ensayo de Materiales , Animales , Bioimpresión , Andamios del Tejido/química , Impresión Tridimensional , Tamaño de la PartículaRESUMEN
Aim: To determine the effect of safranal on diabetic retinopathy in vitro and its possible mechanisms. Methods: We used human retinal microvascular endothelial cells (HRMECs) to test the influence of safranal in vitro. High glucose damage was established and an safranal was tested at various concentrations for its potential to reduce cell viability using the MTT assay. We also employed apoptosis detection, cell cycle detection, a transwell test, and a tube formation assay to look into safranal's inhibitory effects on high glucose damage at various doses. Furthermore, mRNA transcriptome sequencing was performed. mRNA expression levels in a high glucose damage model, a high glucose damage model treated with safranal, and a blank control were compared to find the possible signaling pathway. Western blotting was used to confirm the expressions of several molecules and the levels of phosphorylation in each for the newly discovered pathway. Results: Cell proliferation was inhibited under a high glucose condition but could be protected by safranal at different concentrations (P<0.001). Flow cytometry results suggested safranal also protected cells from apoptosis (P=0.006). A transwell test demonstrated reduced invasiveness of safranal-treated cells in a high glucose condition (P<0.001). In a tube formation investigation, there were noticeably more new branches in the high gloucose group compared to a high glucose treated with safranal group (P<0.001). In mRNA expression patterns on transcriptome sequencing, the MAPK signaling pathway showed an expression ratio. With western blotting, the phosphorylation level of p38-AKT was elevated under a high glucose condition but could be inhibited by safranal. The expression of molecules associated with cell adhesion, including E-cadherin, N-cadherin, Snail, Twist, and fibronectin also changed significantly after safranal treatment under a high glucose condition. Conclusion: Safranal can protect diabetic retinopathy in vitro, and the p38-AKT signaling pathway was found to be involved in the pathogenesis of diabetic retinopathy and could be inhibited by safranal. This pathway may play a role by influencing cell migration and adhesion.