Platelet-Rich Plasma Inhibits Mechanically Induced Injury in Chondrocytes

被引:28
作者
Xie, Xuetao [1 ,2 ]
Ulici, Veronica [1 ]
Alexander, Peter G. [1 ]
Jiang, Yangzi [1 ]
Zhang, Changqing [2 ]
Tuan, Rocky S. [1 ]
机构
[1] Univ Pittsburgh, Ctr Cellular & Mol Engn, Dept Orthopaed Surg, Sch Med, Pittsburgh, PA 15219 USA
[2] Shanghai Jiao Tong Univ, Dept Orthopaed Surg, Affiliated Peoples Hosp 6, Shanghai 200030, Peoples R China
关键词
HUMAN ARTICULAR-CARTILAGE; IN-VITRO; KNEE OSTEOARTHRITIS; HYALURONIC-ACID; NITRIC-OXIDE; TISSUE; COMPRESSION; DEGRADATION; HOMEOSTASIS; TRIAL;
D O I
10.1016/j.arthro.2015.01.007
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
100224 [整形外科学];
摘要
Purpose: To investigate the effect of platelet-rich plasma (PRP) on mechanically injured chondrocytes. Methods: PRP from bovine whole blood was activated to prepare platelet-rich plasma releasate (PRPr). Bovine articular chondrocytes were subjected to 16%, 0.5-Hz biaxial cyclic tensile strain (CTS) for 48 hours and cultured for another 24 hours without cell stretching as an in vitro model of mechanically injured chondrocytes. Culture medium in the 3 PRP-and CTS-treated groups was supplemented with 10% PRPr at the start of CTS, after 24 hours of CTS, and after 48 hours of CTS, respectively. Gene expression levels of type II collagen, aggrecan, matrix metalloproteinase (MMP)-3, MMP-13, inducible nitric oxide synthase, and cyclooxygenase 2 were quantitatively evaluated. Changes in the content of nitric oxide (NO), prostaglandin E2 (PGE(2)), MMP-3, and tissue inhibitor of metalloproteinase 1 in the culture medium were also measured. Results: PRPr increased type II collagen and aggrecan messenger RNA expression; diminished CTS-dependent up-regulation of MMP-3, inducible nitric oxide synthase, and cyclooxygenase 2 gene expression; and reduced CTS-induced overproduction of NO and PGE(2) when PRPr was applied early at the start of CTS. The addition of PRPr after 24 hours of CTS only inhibited MMP-3 gene up-regulation and the increase of NO and PGE(2) induced by CTS. These changes were not observed when PRPr was supplemented after 48 hours of CTS. PRPr mitigated the increased MMP-3 production and decreased tissue inhibitor of metalloproteinase 1 secretion resulting from CTS in a time-dependent manner. Conclusions: PRP treatment ameliorated multiple CTS-mediated catabolic and inflammatory responses in chondrocytes. More beneficial effects were observed with early PRP application.
引用
收藏
页码:1142 / 1150
页数:9
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