No abstract

Abdominal adhesion is a common complication after surgery, which causes pain to patient and increases the risks of reoperation. Electrospinning polyester membrane serving as a physical barrier is used for preventing abdominal adhesion; however, the efficacy is limited due to the lacking of bioactivity necessary for antiadhesion. Here, hydrophobic poly(l‐lactide‐co‐caprolactone) (PLCL) electrospinning membranes are hydrophilized with photo‐crosslinked methacrylic anhydride gelatin (GelMA) hydrogel for postoperative abdominal adhesion prevention. The composite membranes show fibrous network architecture, good cytocompatibility, and hydrophilicity than commercial poly(d,l‐lactide acid) (PDLLA) film. Importantly, the composite membrane provides superior antiadhesion effect over PLCL membrane alone or commercial PDLLA film, against abdominal wall–cecum adhesion models in Sprague Dawley (SD) rats. The underlying mechanism is that PLCL/GelMA membrane successfully promotes the secretion of matrix metalloproteinases 9 (MMP‐9) that can reduce the collagen deposition in extracellular matrix (ECM). Furthermore, the composite membrane significantly upregulates the expression of tissue‐type plasminogen activator (t‐PA) and downregulates the production of plasminogen activator inhibitor‐1 (PAI‐1), leading to the activation of fibrinolytic system, which inhibits the formation of adhesive tissues. Collectively, gelatinized PLCL electrospun membrane is a promising bioactive barrier for preventing postsurgery abdominal adhesions.

No abstract

The treatment of myocardial infarction (MI) remains a substantial challenge due to excessive inflammation, massive cell death, and restricted regenerative potential, leading to maladaptive healing process and eventually heart failure. Current strategies of regulating inflammation or improving cardiac tissue regeneration have limited success. Herein, a hybrid hydrogel coassembled by acellular cardiac extracellular matrix (ECM) and immunomodulatory glycopeptide is developed for endogenous tissue regeneration after MI. The hydrogel constructs a niche recapitulating the architecture of native ECM for attracting host cell homing, controlling macrophage differentiation via glycopeptide unit, and promoting endotheliocyte proliferation by enhancing the macrophage‐endotheliocyte crosstalk, which coordinate the innate healing mechanism for cardiac tissue regeneration. In a rodent MI model, the hybrid hydrogel successfully orchestrates a proreparative response indicated by enhanced M2 macrophage polarization, increased angiogenesis, and improved cardiomyocyte survival, which alleviates infarct size, improves wall thicknesses, and enhances cardiac contractility. Furthermore, the safety and effectiveness of the hydrogel are demonstrated in a porcine MI model, wherein proteomics verifies the regulation of immune response, proangiogenesis, and accelerated healing process. Collectively, the injectable composite hydrogel serving as an immunomodulatory niche for promoting cell homing and proliferation, inflammation modulation, tissue remodeling, and function restoration provides an effective strategy for endogenous cardiac repair.