One of the main illnesses that put people's health in jeopardy is myocardial infarction (MI). After MI, damaged or dead cells set off an initial inflammatory response that thins the ventricle wall and degrades the extracellular matrix. At the same time, the ischemia and hypoxic conditions resulting from MI lead to significant capillary obstruction and rupture, impairing cardiac function and reducing blood flow to the heart. Therefore, attenuating the initial inflammatory response and promoting angiogenesis are very important for the treatment of MI. Here, to reduce inflammation and promote angiogenesis in infarcted area, we report a new kind of injectable hydrogel composed of puerarin and chitosan via self-assembly with simultaneous delivery of mesoporous silica nanoparticles (CHP@Si) for myocardial repair. On the one hand, puerarin degraded from CHP@Si hydrogel modulated the inflammatory response via inhibiting M1-type polarization of macrophages and expression of pro-inflammatory factors. On the other hand, silica ions and puerarin released from CHP@Si hydrogel showed synergistic activity to improve the cell viability, migration and angiogenic gene expression of HUVECs in both conventional and oxygen/glucose-deprived environments. It suggests that this multifunctional injectable CHP@Si hydrogel with good biocompatibility may be an appropriate candidate as a bioactive material for myocardial repair post-MI.
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http://dx.doi.org/10.1093/rb/rbad036 | DOI Listing |
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Department of Cadre Ward, The First Affiliated Hospital of Harbin Medical University, No. 23, Postal Street, Harbin, 150001, Heilongjiang, PR China.
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Students' Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
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Semin Immunopathol
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View Article and Find Full Text PDFSci Rep
January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
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