Micro-current stimulation could inhibit IL-1-induced inflammatory responses in chondrocytes and protect knee bone cartilage from osteoarthritis

BIOMEDICAL ENGINEERING LETTERS(2024)

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摘要
This study aimed to evaluate the inhibitory effects of micro-current stimulation (MCS) on inflammatory responses in chondrocytes and degradation of extracellular matrix (ECM) in osteoarthritis (OA). To determine the efficacy of MCS, IL-1 beta-treated chondrocytes and monosodium iodoacetate (MIA)-induced OA rat model were used. To evaluate the cytotoxicity and nitric oxide (NO) production in SW1353 cells, the presence or absence of IL-1 beta treatment or various levels of MCS were applied. Immunoblot analysis was conducted to evaluate whether MCS can modulate IL-1R1/MyD88/NF-kappa B signaling pathway and various indicators involved in ECM degradation. Additionally, to determine whether MCS alleviates subchondral bone structure destruction caused by OA, micro-CT analysis, immunoblot analysis, and ELISA were conducted using OA rat model. 25 and 50 mu A levels of MCS showed effects in cell proliferation and NO production. The MCS group with IL-1 beta treatment lead to significant inhibition of protein expression levels regarding IL-1R1/MyD88/NF-kappa B signaling and reduction of the nucleus translocation of NF-kappa B. In addition, the protein expression levels of MMP-1, MMP-3, MMP-13, and IL-1 beta decreased, whereas collagen II and aggrecan increased. In animal results, morphological analysis of subchondral bone using micro-CT showed that MCS induced subchondral bone regeneration and improvement, as evidenced by increased thickness and bone mineral density of the subchondral bone. Furthermore, MCS-applied groups showed decreases in the protein expression of MMP-1 and MMP-3, while increases in collagen-II and aggrecan expressions. These findings suggest that MCS has the potential to be used as a non-pharmaceutical method to alleviate OA.
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关键词
Micro-current stimulation,Osteoarthritis,Chondrocytes,Articular cartilage,IL-1 beta/MyD88/NF-kappa B signaling
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