Abstract
Therapeutic effects of GCSB-5 on osteoarthritis were measured by the amount of glycosaminoglycan in rabbit articular cartilage explants in vitro, in experimental osteoarthritis induced by intra-articular injection of monoiodoacetate in rats in vivo. GCSB-5 was orally administered for 28 days. In vitro, GCSB-5 inhibited proteoglycan degradation. GCSB-5 significantly suppressed the histological changes in monoiodoacetate-induced osteoarthritis. Matrix metalloproteinase (MMP) activity, as well as, the levels of serum tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide synthase protein, and mRNA expressions were attenuated by GCSB-5, whereas the level of interleukin-10 was potentiated. By GCSB-5, the level of nuclear factor-κB p65 protein expression was significantly attenuated but, on the other hand, the level of inhibitor of κB-α protein expression was increased. These results indicate that GCSB-5 is a potential therapeutic agent for the protection of articular cartilage against progression of osteoarthritis through inhibition of MMPs activity, inflammatory mediators, and NF-κB activation.
Highlights
Osteoarthritis (OA) is a degenerative joint disease characterized by joint pain and a progressive loss of articular cartilage
GCSB-5 was further standardized for quality control according to the regulations imposed by Korea Food and Drug Administration (KFDA)
Our results indicate that GCSB-5 inhibits collagen degradation through inhibition of Matrix metalloproteinase (MMP)-2 and -9 activities in late stage of OA
Summary
Osteoarthritis (OA) is a degenerative joint disease characterized by joint pain and a progressive loss of articular cartilage. Developing therapeutics from herbal sources may reduce the risk of toxicity or adverse effects when the drug is clinically used [5] and may exert strong, multifunctional anti-inflammatory effect like many natural products do. Eucommiae Cortex exhibits strong analgesic effect [15] and geniposide from its extract shows anti-inflammatory effect on rheumatoid arthritis rats [16] and enhances the osteoblast-like cell proliferation and inhibited osteoclast [17]. GCSB-5 reduces the development of acute and chronic inflammation, and its anti-inflammatory property is likely due to inhibition of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression via downregulation of the Akt signal pathway and inhibition of nuclear factor-κB (NF-κB) activation [18]. We examined the chondroprotective and anti-inflammatory effects of GCSB-5 on monoiodoacetate (MIA)-induced OA animal model, both in vitro and in vivo
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