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Effects and mechanism of sestrin1 protein on osteoarthritis inflammation: A cellular model study
Yawei Wu1, Xiaoying Liang1, Yuyan Yang1
1Affiliated Traditional Chinese Medicine Hospital of Xinjiang Medical University, Urumqi City, China.
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.
