Polyglycolic acid (PGA)/hyaluronic acid (HA) biomaterial |
|
[180] |
Alginate hydrogel |
Human chondrocytes cultured into alginate beads in the presence of H-PRP 3 expressed significantly higher amounts of type I collagen (COL1A1) compared to cells maintained into biomaterials and treated with a medium supplemented with OA-PRP 4
OA-PRP had a greater ability to induce a proinflammatory response in human macrophages compared to H-PRP
|
[181] |
Collagen-based hydrogel |
It was demonstrated that the GAG/DNA content was significantly higher in the group supplemented with PRP 1 compared with the group without supplementation during 21 days of incubation
An in vivo study on rabbits using BMSCs 5-collagen hydrogel constructs, which were implanted followed by a PRP 1 intra-articular injection, showed that such a construct inhibited fibrocartilage formation, promoted GAG and collagen synthesis and enhanced faster cartilage healing
|
[182] |
3D porous silk-fibroin (3D SF) biomaterial fabricated using salt-leaching technique |
Human ADSCs 6 cultured on biomaterial in a medium supplemented with PRP possessed the highest ability to proliferate in comparison with cells grown on a scaffold both in a medium with 10% FBS as well as a chondrogenic medium
A medium with the addition of PRP significantly enhanced the production of TGF-β1, total protein and GAGs 6 by ADSCs 6 cultured on a 3D SF scaffold when compared to both control media
|
[183] |
3D porous silk-fibroin (3D SF) biomaterial fabricated using salt-leaching-technique SF biomaterial |
Human ADSCs 6 which were grown on a 3D SF scaffold in a medium supplemented with LAA 7 or PRP 1 possessed a higher ability to produce GAGs 6 when compared to cells grown on such scaffold in a basal medium
After 7 and 21 days of incubation, it was shown that both LAA 7 and PRP 1 were similarly responsible for the increased expression of N-cadherin (CDH2) and COL2A1 in ADSCs 6 grown on a silk-fibroin-based scaffold. Moreover, on day 21, the presence of PRP 1 in the culture medium was also able to inhibit the expression of β-catenin (CTNNB1) and cyclin D (CCND1) in these cells, which is clear evidence of chondrogenic differentiation support.
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[183,184] |