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Acteoside Counteracts Interleukin-1β-Induced Catabolic Processes through the Modulation of Mitogen-Activated Protein
HyangI Lim1, Do Kyung Kim1, Tae-Hyeon Kim1
1Institute of Dental Science, Chosun University, Gwangju 61452, Republic of Korea.
Abstract:
Osteoarthritis (OA) is the most common degenerative joint disease with chronic joint pain caused by progressive degeneration of articular cartilage at synovial joints. Acteoside, a caffeoylphenylethanoid glycoside, has various biological activities such as antimicrobial, anti-inflammatory, anticancer, antioxidative, cytoprotective, and neuroprotective effect. Further, oral administration of acteoside at high dosage does not cause genotoxicity. Therefore, the aim of present study is to verify the anticatabolic effects of acteoside against osteoarthritis and its anticatabolic signaling pathway. Acteoside did not decrease the viabilities of mouse fibroblast L929 cells used as normal cells and primary rat chondrocytes. Acteoside counteracted the IL-1β-induced proteoglycan loss in the chondrocytes and articular cartilage through suppressing the expression and activation of cartilage-degrading enzyme such as matrix metalloproteinase- (MMP-) 13, MMP-1, and MMP-3. Furthermore, acteoside suppressed the expression of inflammatory mediators such as inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, and prostaglandin E2 in the primary rat chondrocytes treated with IL-1β. Subsequently, the expression of proinflammatory cytokines was decreased by acteoside in the primary rat chondrocytes treated with IL-1β. Moreover, acteoside suppressed not only the phosphorylation of mitogen-activated protein kinases in primary rat chondrocytes treated with IL-1β but also the translocation of NFκB from the cytosol to the nucleus through suppression of its phosphorylation. Oral administration of 5 and 10 mg/kg acteoside attenuated the progressive degeneration of articular cartilage in the osteoarthritic mouse model generated by destabilization of the medial meniscus. Our findings indicate that acteoside is a promising potential anticatabolic agent or supplement to attenuate or prevent progressive degeneration of articular cartilage.
Insights
Acteoside, a natural compound, shows promise in preventing osteoarthritis progression. It counteracts cartilage degradation and inflammation by inhibiting key enzymes and signaling pathways, offering a potential therapeutic supplement.
Area of Science:
- Biochemistry
- Pharmacology
- Biomaterials
Background:
- Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by articular cartilage breakdown and chronic pain.
- Acteoside, a caffeoylphenylethanoid glycoside, exhibits diverse biological activities, including anti-inflammatory and antioxidative effects, with no observed genotoxicity upon oral administration.
- Understanding the anticatabolic mechanisms of acteoside is crucial for developing novel OA treatments.
Purpose of the Study:
- To investigate the anticatabolic effects of acteoside on osteoarthritis.
- To elucidate the underlying anticatabolic signaling pathways influenced by acteoside.
Main Methods:
- In vitro studies using mouse fibroblast L929 cells and primary rat chondrocytes to assess cytotoxicity and protective effects.
- Analysis of proteoglycan loss, cartilage-degrading enzymes (MMP-13, MMP-1, MMP-3), inflammatory mediators (iNOS, COX-2, NO, PGE2), and pro-inflammatory cytokines.
- Investigation of signaling pathways, including mitogen-activated protein kinases (MAPKs) and NFκB translocation.
- In vivo studies using an osteoarthritis mouse model induced by destabilization of the medial meniscus (DMM).
Main Results:
- Acteoside demonstrated no cytotoxicity to normal cells and chondrocytes.
- It effectively counteracted IL-1β-induced proteoglycan loss and suppressed cartilage-degrading enzymes (MMP-13, MMP-1, MMP-3).
- Acteoside inhibited inflammatory mediators and pro-inflammatory cytokines, suppressed MAPK phosphorylation, and prevented NFκB translocation.
- Oral administration of acteoside attenuated articular cartilage degeneration in an OA mouse model.
Conclusions:
- Acteoside exhibits significant anticatabolic effects against osteoarthritis progression.
- It acts by suppressing cartilage degradation, inflammation, and key signaling pathways.
- Acteoside represents a promising therapeutic agent or supplement for managing osteoarthritis.
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