Protectin DX attenuates IL-1β-induced inflammation via the AMPK/NF-κB pathway in chondrocytes and ameliorates osteoarthritis progression in a rat model.
Human chondrocyte cell lines, CHON-001 and ATDC5, were treated with different doses of interleukin-1β (IL-1β) to simulate the inflammatory response environment of OA. miR-138-5p mimics, miR-138-5p inhibitors and SOX9 small interfering RNA (siRNA) were constructed and transfected into CHON-001 and ATDC5 cells.
To analyze the correlation between the Kellgren-Lawrence (K-L) score of knee osteoarthritis (KOA) patients with different degrees and their urine concentration of C-terminal telopeptide of collagen type II (CTX-II) and interleukin-1β (IL-1β), and to further evaluate the diagnostic value of CTX-II and IL-1β during the pathological process by producing an experimental osteoarthritis (OA) model in rabbits.
Then, we revealed in interleukin 1β (IL-1β)-induced OA chondrocytes in vitro that pretransfection with miR-140 effectively inhibited the expression of SA-βGal, p16<sup>INK4a</sup>, p21, p53, and γH2AX.
Subsequently, we further verified in vivo that exogenous injection of AOPPs in OA mice up-regulated expression of TNF-α and IL-1β in cartilage, which was blocked by treatment with apocynin.
The results showed that, compared to the OA group, the OA + treadmill and OA + wheel groups had lower levels of IL-1β, IL-6 and TNF-α, and similar levels of p-P65, p-JNK, and P-IκBα.
Taken together, we identified a critical role of SGK1 in the IL-1β-induced chondrocyte anabolic and catabolic imbalance, which may represent a potential novel therapeutic target for OA.
The effect of DAP on primary rabbit chondrocytes was examined using recombinant human IL-1β for 24 h. For the in vivo studies, rabbits were randomly divided into groups: a normal control group and osteoarthritis (OA) groups.
Furthermore, COL2A1 knockdown reversed the effects of miR-455-3p inhibition, and aggravated the effects of miR-455-3p overexpression on IL-1β-induced OA-like phenomenon.
In general, the data indicate that Peimine suppresses IL‑1β‑induced inflammation in mouse chondrocytes by inhibiting the MAPK pathway, suggesting a promising therapeutic role for Peimine in the treatment of OA.
To simulate osteoarthritis in vitro, human articular cartilage explants were placed in culture and treated with IL-1β, a cytokine with known cartilage catabolic and pro-inflammatory effects.
In this study, we investigated the inhibitory property of metformin on mitochondrial damage by focusing on the interleukin-1 beta (IL-1β)-stimulated osteoarthritis model by using primary murine chondrocytes.
Glo-1 is impaired by inflammation mediated by IL-1β in chondrocytes through oxidative stress pathways and may explain age-dependent accumulation of the AGE CML in OA cartilage.
Osteoarthritis (OA) is a degenerative condition that involves the production of inflammatory cytokines (e.g., interleukin-1β (IL-1β), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6)) that stimulate degradative enzymes, matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS) resulting in articular cartilage breakdown.
In this study, the human chondrosarcoma cell line SW1353 was cultured in vitro, and an OA cell model was constructed with inflammatory factor IL-1β stimulation.
After knockdown of PHF23, the level of autophagy-related proteins increased and apoptotic-related proteins decreased in IL-1β-induced OA-like chondrocytes.
The quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expressions of LINC01534, aggrecan, collagen II, and matrix metalloproteinase (MMPs) in OA cartilage tissue or OA chondrocyte model induced by IL-1β.
CONCLUSIONS Our work suggested that catalpol treatment attenuates IL-1ß-induced inflammatory response and catabolism in rat chondrocytes by inhibiting the NF-kappaB pathway, suggesting the therapeutic potential of catalpol for the treatment of osteoarthritis.
We have previously reported that chondroitin sulfate extracted from Sturgeon bone (CSSB) can alleviate the pain caused by osteoarthritis (OA) by reducing the expression of matrix metalloproteinases (MMPs) and inflammatory factors (IL-1, TNF-α and PGE<sub>2</sub>).
Astragaloside inhibits IL-1β-induced inflammatory response in human osteoarthritis chondrocytes and ameliorates the progression of osteoarthritis in mice.