We assessed the effects of pulsed electromagnetic field (PEMF) on cartilage degeneration, and expression of mitogen-activated protein kinases (MAPKs) and matrix metalloproteinases (MMPs), in an experimental rat model of osteoarthritis induced by anterior cruciate ligament transection (ACLT).
Experimental.
University animal laboratory.
30 male Sprague-Dawley rats.
We performed histological examination, enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, to assess cartilage degeneration, urine C-terminal cross-linking telopeptide of type II collagen (CTX-II), and mRNA expression of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (c-Jun), p38, and MMPs.
Urinary CTX-II in the PEMF group was significantly lower than in the ACLT group at 9 and 13 weeks. Mankin scores in the PEMF group significantly lower than that in the ACLT group (P < 0.01). mRNA expression of ERK1, c-Jun, p38, MMP-13 and MMP-3 was significantly higher in the ACLT group than in the Sham group, while that with the sole exception of MMP-3 in the PEMF group was significantly lower than in the ACLT group.
PEMF may regulate the catabolic factor, MMP13, and inhibit cartilage destruction, at least partially, by inhibiting MAPKs signaling pathway.