LncRNA NKILA attenuates the progression of osteoarthritis through the targeted inhibition of the NF-κB pathway

Background: Interleukin-1 beta (IL-1 beta) plays a crucial role in cartilage degeneration by inducing inflammatory cascades in chondrocytes, impairing their normal biological functions. Long non-coding RNA NKILA (lncRNA NKILA) has been implicated in osteoarthritis (OA), but its specific molecular mechanisms remain unclear. This study aims to elucidate the function and molecular regulatory mechanism of lncRNA NKILA in articular chondrocytes under IL-1 beta stimulation. Methods: Primary human articular chondrocytes were cultured to investigate the effects of IL-1 beta on chondrocyte proliferation, apoptosis, and extracellular matrix metabolism. We employed Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR), western blot, flow cytometry, immunofluorescence, and nuclear mass separation assays to explore the interaction between lncRNA NKILA and the NF kappa B signaling pathway. Additionally, animal experiments were conducted to evaluate the therapeutic potential of modulating lncRNA NKILA expression in vivo. Results: IL-1 beta treatment led to decreased chondrocyte proliferation and increased apoptosis. Our study demonstrated that IL-1 beta downregulates lncRNA NKILA, which weakens its inhibitory effect on the NF kappa B (Nuclear Factor Kappa B) signaling pathway. This downregulation results in increased NF kappa B activity and exacerbates chondrocyte degeneration. Notably, the upregulation of lncRNA NKILA significantly alleviated OA symptoms, indicating that NKILA could be a promising therapeutic target. Conclusion: IL-1 beta reduces lncRNA NKILA expression, weakening its inhibition of NF kappa B signaling and promoting articular chondrocyte degeneration. Enhancing lncRNA NKILA expression offers a promising approach to mitigating OA, suggesting that NKILA could serve as a potential therapeutic target for OA treatment.