acteoside and Osteoarthritis

Topics: Animals; Anti-Inflammatory Agents; Cartilage, Articular; Cell Line; Cells, Cultured; Chondrocytes; Cyclooxygenase 2; Dinoprostone; Glucosides; Immunosuppressive Agents; Interleukin-1beta; Matrix Metalloproteinases; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Osteoarthritis; Phenols; Rats; Rats, Sprague-Dawley; Signal Transduction

BACKGROUND Cartilage degeneration during osteoarthritis (OA) most adversely affects the quality of life by hindering the movement. The present study investigated the role of verbascoside in the protection of cartilage degeneration induced by osteoarthritis. MATERIAL AND METHODS The enzyme-linked immunosorbent (ELISA) and western blot assays were used for determination of inflammatory cytokine secretion in serum and cartilage tissues, respectively. RESULTS Treatment of the OA rats with verbascoside inhibited overproduction of interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and IL-1ß in serum as well as cartilage tissues. The expression of P2X7R and matrix metalloproteinase (MMP)-13 was much higher in the rats induced with OA. However, administration of verbascoside reversed the OA-induced upregulation of P2X7R and MMP-13 expression in the cartilage tissues. The OA-mediated increase in substance P (SP) and prostaglandin E2 (PGE2) expression was also reduced in the cartilage tissues by the verbascoside treatment. Western blot assay revealed that verbascoside treatment markedly decreased the activation of IkappaBalpha and NF-kappaB p65 in the OA rats. CONCLUSIONS Thus, verbascoside inhibited inflammatory cytokine secretion in the OA rats by targeting P2X7R expression, production of matrix metalloproteinase, PGE2 and downregulation of NF-kappaB signaling pathway. Therefore, verbascoside may be used as potent agent for osteoarthritis treatment.

Topics: Animals; Cartilage, Articular; Cytokines; Disease Models, Animal; Down-Regulation; Glucosides; Immunosuppressive Agents; NF-kappa B; Osteoarthritis; Phenols; Purinergic P2X Receptor Antagonists; Quality of Life; Rats

Osteoarthritis (OA) is a common degenerative disease of synovial joints caused by inflammation. Acteoside (ACT), a major component and lipase inhibitor from the Chinese tea Ligustrum purpurascens kudingcha, has been reported to regulate the inflammation and immune response. The study aims to investigate the effects of ACT on inflammatory responses and joint protection in OA rats.. Cell proliferation was examined by MTT and colony formation assay. Apoptosis was analyzed using flow cytometry with Annexin V/PI staining. ELISA was employed to examine the concentration of inflammatory cytokines. OA rat model was established by surgery stimulation.. ACT treatment significantly inhibited the upregulation of inflammatory cytokines induced by IL-1β in primary chondrocytes, including IL-6, IL-12, TNF-α and IFN-γ. ACT stimulation also enhanced the cell proliferation, while inhibited cell apoptosis in IL-1β-treated chondrocytes. Consistently, ACT treatment led to downregulation of cleaved-caspase-3 and apoptosis regulator Bax, and upregulation of Bcl-2. Furthermore, ACT treatment inhibited IL-1β-induced activation of JAK/STAT pathway. The results were confirmed in surgery-induced OA rat model. Moreover, ACT treatment significantly inhibited synovial inflammation and articular chondrocyte apoptosis in OA rats.. Our findings indicate that ACT has the potential therapeutic effect on OA through inhibiting the inflammatory responses via inactivating JAK/STAT signaling pathway.

Topics: Animals; Cell Proliferation; Chondrocytes; Disease Models, Animal; Drugs, Chinese Herbal; Glucosides; Humans; Interferon-gamma; Janus Kinases; Ligustrum; Male; Osteoarthritis; Phenols; Rats; Rats, Sprague-Dawley; Signal Transduction; STAT Transcription Factors; Tumor Necrosis Factor-alpha