Effects and mechanism of sestrin1 protein on osteoarthritis inflammation: A cellular model study.

BACKGROUND: Knee osteoarthritis is characterized by inflammation, oxidative injury, and degeneration of cartilage. Approximately 30% of people over 45 years old exhibit radiographic signs of knee osteoarthritis, with symptoms present in roughly half of these cases. Novel non-pharmacological interventions play a critical role in the management of knee osteoarthritis. In the present study, an exercise-induced protein, sestrin1, was investigated to clarify the effects and mechanism of sestrin1 protein in osteoarthritis inflammation. METHODS: A cellular osteoarthritis model was established using IL-1β-induced ATDC5 cells. The expression level of the sestrin1 protein was examined via a QRT-PCR experiment. Sestrin1 was knocked down in the cellular osteoarthritis model to evaluate its impact on inflammation and the AMPK-mTORC1 signaling pathway. Data were presented as mean ± SD. The t-test and one-way ANOVA were used for the comparison. RESULTS: Sestrin1 expression was upregulated in cellular osteoarthritis models; TNF-α, IL-18, IL-6, and IL-1β were exacerbated when sestrin1 was silenced; The AMPK-mTORC1-NF-κB signaling axis was involved in this process, with sestrin1 acting as an activator of AMPK. CONCLUSIONS: Sestrin1 was upregulated in a cellular osteoarthritis model and played a critical role in regulating inflammation and lesions, partially through the AMPK-mTORC1-NF-κB pathway.