The therapeutic effect of aucubin-supplemented hyaluronic acid on interleukin-1beta-stimulated human articular chondrocytes
| Autor: | Jo Yu Liao, Shu-Hua Yang, Teng Le Huang, Yun Tang, Kai Chiang Yang, Yi Ru Chen |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Cartilage
Articular Cell Survival Interleukin-1beta Iridoid Glucosides Pharmaceutical Science Pharmacology medicine.disease_cause Antioxidants Collagen Type I Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound Chondrocytes 0302 clinical medicine Lactate dehydrogenase Drug Discovery Hyaluronic acid medicine Humans Viability assay Hyaluronic Acid Cells Cultured Aggrecan Aucubin Glycosaminoglycans 030304 developmental biology chemistry.chemical_classification 0303 health sciences Reactive oxygen species biology Tumor Necrosis Factor-alpha Osteoarthritis Knee Complementary and alternative medicine chemistry Cyclooxygenase 2 030220 oncology & carcinogenesis biology.protein Cytokines Molecular Medicine Oxidative stress |
| Zdroj: | Phytomedicine. 53:1-8 |
| ISSN: | 0944-7113 |
| Popis: | Background Injection of exogenous hyaluronic acid (HA) into the joint capsule improves symptoms of early stage osteoarthritis (OA). However, reactive oxygen species degrade HA into small oligosaccharides that can elicit pro-inflammatory responses. Likewise, disturbance of the antioxidant enzyme system and generation of oxidative stress by pro-inflammatory cytokines worsen knee OA. Accordingly, we proposed the use of aucubin, an antioxidant and anti-inflammatory compound, as a versatile adjuvant to HA for treating OA. Methods Primary human chondrocytes were cultured in media supplemented with aucubin in a series of concentrations (0, 0.01, 0.1, 1, and 10 μg/ml) to study dose-dependent toxicity. We then evaluated the therapeutic effects of HA (100 μg/ml) supplemented with aucubin (10 μg/ml) on interleukin-1 beta (IL-1β, 10 ng/ml)-stimulated chondrocytes. Results The use of aucubin did not change cell viability or alter lactate dehydrogenase release to normal chondrocytes. Although the proliferation and sulfated glycosaminoglycan production were not affected, aucubin partially restored the hypertrophic transformation of chondrocytes. Relative to treatment with HA or aucubin alone, real-time PCR revealed that aucubin-supplemented HA down-regulated the mRNA levels of tumor necrosis factor-alpha (TNF-α), corrected collagen type 1 and aggrecan, and up-regulated tissue inhibitor of metalloproteinase 1. Moreover, ELISA testing also showed a reduced TNF-α production. Although superoxide dismutases activity was still distributed, aucubin restored total antioxidant capacity of IL-1β-stimulated chondrocytes. Western blotting further showed that aucubin inhibited cyclooxygenase-2 and regulated the nuclear factor (erythroid-derived 2)-like 2 pathway. Conclusion Aucubin can enhance the anti-catabolic and anti-inflammatory effects of HA on OA chondrocytes. |
| Databáze: | OpenAIRE |
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