Micro-current stimulation could inhibit IL-1β-induced inflammatory responses in chondrocytes and protect knee bone cartilage from osteoarthritis.
Minjoo LeeHana LeeHalim ChungJin-Ho LeeDoyong KimSeungkwan ChoTack-Joong KimHan Sung KimPublished in: Biomedical engineering letters (2024)
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-1β-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-1β treatment or various levels of MCS were applied. Immunoblot analysis was conducted to evaluate whether MCS can modulate IL-1R1/MyD88/NF-κB 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 µA levels of MCS showed effects in cell proliferation and NO production. The MCS group with IL-1β treatment lead to significant inhibition of protein expression levels regarding IL-1R1/MyD88/NF-κB signaling and reduction of the nucleus translocation of NF-κB. In addition, the protein expression levels of MMP-1, MMP-3, MMP-13, and IL-1β 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.
Keyphrases
- bone mineral density
- extracellular matrix
- signaling pathway
- knee osteoarthritis
- bone regeneration
- postmenopausal women
- pi k akt
- cell proliferation
- nitric oxide
- high glucose
- body composition
- computed tomography
- induced apoptosis
- rheumatoid arthritis
- lps induced
- diabetic rats
- oxidative stress
- soft tissue
- toll like receptor
- magnetic resonance imaging
- nuclear factor
- cell cycle arrest
- hydrogen peroxide
- contrast enhanced
- cell cycle
- positron emission tomography
- inflammatory response
- anterior cruciate ligament reconstruction
- data analysis
- monoclonal antibody