Silencing BLNK protects against interleukin-1β-induced chondrocyte injury through the NF-κB signaling pathway

Background: Osteoarthritis (OA) is the most common joint disease in the elderly and is characterized by the progressive degeneration of articular cartilage. It is necessary to study the molecular pathology of OA. This study aimed to explore the role and mechanism of BLNK in regulating interleukin-1 beta (IL-1 beta)-induced chondrocyte injury and OA progression. Methods: GSE1919 (5 normal samples and 5 OA samples) was downloaded from the Gene Expression Omnibus (GEO) database. The limma package in R software was used to identify differentially expressed genes (DEGs) between control and OA-affected cartilage. Gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of the differentially expressed genes were also performed. Apoptosis was assessed by flow cytometry. An OA rat model was established, and the relative expression of BLNK was assessed by real time quantitative PCR (qRT-PCR) and immunohistochemical staining. The expression of collagen II, MMP9, p65 and p-p65 was measured by Western blot analysis. Moreover, inflammatory factors (TNF-alpha and IL-18) were assessed by ELISA. The NF-Kappa B inhibitor JSH-23 was used to assess the impact of BLNK on the NF-Kappa B signaling pathway. Results: In total, 1318 DEGs were identified between normal and OA-affected cartilage according to the criteria (P-value <0.05 and |logFC > 1|). These DEGs were mainly enriched in the NF-Kappa B pathway. BLNK was highly expressed in OA cartilage tissue and injured chondrocytes. Silencing BLNK significantly downregulated the IL-1 beta induced apoptosis of chondrocytes. Silencing BLNK partially increased collagen II expression and downregulated MMP13 expression. Moreover, silencing BLNK partially decreased TNF-alpha and IL-18 expression. BLNK silencing inhibited the activation of NF-Kappa B in OA. Silencing BLNK delayed OA progression through the NF-Kappa B signaling pathway. Conclusion: Silencing BLNK delayed OA progression and IL-1 beta-induced chondrocyte injury by regulating the NF Kappa B pathway.