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EGb761 inhibits inflammatory responses in human chondrocytes and shows chondroprotection in osteoarthritic rat knee
- Source :
- Journal of orthopaedic research : official publication of the Orthopaedic Research Society. 31(7)
- Publication Year :
- 2012
-
Abstract
- Osteoarthritis (OA) is a degenerative joint disease involving a combination of cartilage degradation and inflammation. EGb761, a standardized extract of Ginkgo biloba leaves, holds an anti-inflammatory potency. Here, we determined whether EGb761 could inhibit lipopolysaccharide (LPS)- and IL-1β-induced inflammatory responses in human articular chondrocytes and apply the chondroprotection in OA rats. We found that LPS markedly induced the productions of PGE2 and NO and the protein expressions of COX-2 and iNOS in human chondrocytes. LPS was also seen to up-regulate the expressions of toll-like receptor-4 (TLR4), its downstream signal TNF receptor-associated factor 6 (TRAF6), and nuclear factor (NF)-κB signaling. These LPS-induced inflammatory responses were efficaciously reversed by EGb761 and its active components quercetin and kampferol. The similar results could be observed by using IL-1β as an in vitro model to mimic an inflammatory response. In an OA rat model, PGE2 and NO levels in blood, the histological alterations, and COX-2 and nitrotyrosine expressions in cartilages were markedly increased, which were effectively reversed by EGb761. Our results suggested that EGb761 exerts the anti-inflammatory effects on human articular chondrocytes and OA rats.
- Subjects :
- Lipopolysaccharides
Male
Plant Extracts
Interleukin-1beta
NF-kappa B
Ginkgo biloba
Nitric Oxide Synthase Type II
Middle Aged
Osteoarthritis, Knee
Nitric Oxide
Dinoprostone
Rats
Toll-Like Receptor 4
Disease Models, Animal
Chondrocytes
Cyclooxygenase 2
Animals
Humans
Tyrosine
Rats, Wistar
Cells, Cultured
Aged
Subjects
Details
- ISSN :
- 1554527X
- Volume :
- 31
- Issue :
- 7
- Database :
- OpenAIRE
- Journal :
- Journal of orthopaedic research : official publication of the Orthopaedic Research Society
- Accession number :
- edsair.pmid..........4ddcf8ea485ae88d30960ae763a2e05b