动物造模 zi-bio 2024-05-06 540

　　Objective: Osteoarthritis is the most common degenerative chronic joint disease, but its specific genetic mechanism is still not fully understood. By using gene chips to detect changes in gene expression profiles of OA cell models, more biological basis is provided for in-depth research on the pathogenesis of OA

　　Method: Mouse primary chondrocytes were isolated by combining trypsin with collagenase, and treated with 50ng/mL of tumor necrosis factor α (TNF)- α) Incubate primary chondrocytes for 24 hours to prepare an OA cell model. Extract total RNA from the harvested cells for gene chip detection, and screen differentially expressed genes (DEGs) under the condition of fold change (FC)>2 and P<0.01. Use bioinformatics software to perform gene function classification system (GO) and KEGG pathway annotation analysis on the differentially expressed results

　　Result: Primary chondrocytes were treated with TNF- α After processing, a total of 8096 upregulated DEGs and 6413 downregulated DEGs were screened, including known differentially expressed genes related to OA, such as matrix metalloproteinases, inflammatory factors, gene apoptosis, and osteogenic genes. In addition, there were also unknown genes related to OA, such as Olfml1 and Nf1, which have not been reported. In particular, a large number of genes related to cytochrome superfamily members were found to have abnormal expression, suggesting that mitochondrial related functional genes and signaling pathways may be closely related to the OA process

　　Conclusion: The project analyzed TNF as a whole at the transcriptome level- α The induced changes in gene expression profile of OA chondrocyte model provide new ideas for further exploring the pathogenesis of OA