Rat Chondrocyte Inflammation and Osteoarthritis Are Ameliorated by Madecassoside.
Safwat Adel Abdo MoqbelYuzhe HeLanghai XuChiyuan MaJisheng RanKai XuLi-Dong WuPublished in: Oxidative medicine and cellular longevity (2020)
As a joint disease, osteoarthritis (OA) is caused by the breakdown of subchondral bone and cartilage damage. Inflammatory factors, such as interleukin- (IL-) 1β, mediate the progression of OA. Madecassoside (MA), a triterpenoid component derived from the gotu kola herb (Centella asiatica), exhibits various pharmacological effects, including antioxidative and anti-inflammatory properties. In the present study, the protective effects and possible mechanism of MA on the treatment of OA were investigated. MA was demonstrated to significantly suppress the IL-1β-induced overexpression of matrix metalloproteinase- (MMP-) 3, MMP-13, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) and to decrease the IL-1β-induced degradation of type II collagen and sox9. Additionally, MA was able to reduce the IL-1β-induced phosphorylation of p65 in osteoarthritic chondrocytes. Furthermore, in a rat OA model, MA prevented cartilage degeneration and reduced the OARSI score in the MA-treated group compared with the OA group. The present study showed that MA suppresses the nuclear factor-κB signaling pathway, reducing IL-1β-induced chondrocyte inflammation, which indicates the therapeutic potential of MA in patients with OA.
Keyphrases
- oxidative stress
- knee osteoarthritis
- diabetic rats
- nitric oxide synthase
- high glucose
- signaling pathway
- nuclear factor
- nitric oxide
- rheumatoid arthritis
- anti inflammatory
- stem cells
- transcription factor
- toll like receptor
- bone mineral density
- pi k akt
- cell proliferation
- endothelial cells
- inflammatory response
- extracellular matrix
- cell migration
- postmenopausal women
- induced apoptosis
- stress induced