AI Article Synopsis
- The study investigates the effects of indomethacin on slowing osteoarthritis (OA) progression by using chondrocyte cells treated with IL-1β, which simulates OA conditions.
- It finds that IL-1β worsens inflammation and other adverse cellular processes in chondrocytes, while indomethacin counteracts these negative effects and inhibits a critical signaling pathway (PI3K/AKT/mTOR).
- The conclusion suggests that indomethacin helps regulate inflammation and cellular processes, potentially slowing down the development of OA by acting on the signaling pathway involved.
Article Abstract
Objective: To elucidate how indomethacin may slow the progression of osteoarthritis (OA).
Methods: Chondrocytes were treated with IL-1β (10 ng/mL) for 12 hours to create an in vitro model of OA. Following this, 10 μM of indomethacin was added to the IL-1β-treated chondrocytes for an additional 4 hours to evaluate its effects on inflammation, anabolism, catabolism, apoptosis, and autophagy using ELISA, western blot, immunofluorescence and flow cytometry, respectively.
Results: IL-1β significantly stimulated inflammatory responses, hampered anabolic processes, induced catabolic activity, accelerated apoptosis, and inhibited autophagy in chondrocytes, as well as activated the PI3K/AKT/mTOR signaling pathway. However, treatment with indomethacin reversed the effects of IL-1β stimulation on chondrocytes and simultaneously suppressed the activation of the PI3K/AKT/mTOR signaling pathway.
Conclusions: Our findings indicate the mechanism of action of indomethacin in mitigating OA progression, indicating that it can inactivate the PI3K/AKT/mTOR signaling pathway, thereby regulating inflammation, metabolism, apoptosis, and autophagy in chondrocytes, which attenuates the development of OA.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11609557 | PMC |
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