动物造模,骨关节炎细胞模型 z-bio 2022-09-13 473

　　OBJECTIVE: Osteoarthritis is the most common degenerative chronic joint disease, but its specific genetic mechanism is still not fully understood. The gene expression profile changes of OA cell models were detected by gene chip to provide more biological resources for the in-depth study of the pathogenesis of OA. Study basis.

　　Methods: Primary mouse chondrocytes were isolated by trypsin combined with collagenase, and primary chondrocytes were incubated with 50ng/mL tumor necrosis factor α (TNF-α) for 24 h to prepare OA cell model. The cells were harvested to extract total RNA for gene chip Differentially expressed genes (DEGs) were screened under the condition of expression difference fold change (FC)>2 and P<0.01, and the differentially expressed results were classified into gene ontology (gene ontology, DEGs) using bioinformatics software. GO), KEGG pathway annotation analysis.

　　RESULTS: After primary chondrocytes were treated with TNF-α, a total of 8096 up-regulated DEGs and 6413 down-regulated DEGs were screened, including known genes such as matrix metalloproteinases, inflammatory factors, apoptosis and osteogenesis-related genes. In addition, there are olfactomedin superfamily members such as Olfml1, Nf1 and other unreported OA-related genes, especially the abnormal expression of a large number of cytochrome superfamily member genes, suggesting that mitochondrial-related functional genes and Signaling pathways may be important in the OA process.

　　Conclusion: The project comprehensively analyzed the gene expression profile changes of OA chondrocyte model induced by TNF-α from the transcriptome level, and provided a new idea for further in-depth exploration of the pathogenesis of OA.