动物造模,沉默miRNA-16对肺结核模型 z-bio 2021-12-28 337

　　Objective: To study the regulation and mechanism of miR-16 silencing on the immune function of pulmonary tuberculosis model mice.

　　Method: Select 40 CD2F1 female mice and divide them into normal group, model group, overexpression group, 10 silence group, model group, overexpression group and silence group to establish tuberculosis model, and successfully model. After that, 10 μL of miR-16 lentivirus suspension was aseptically injected into the lungs of silenced mice in the overexpression group. To detect T lymphocyte subsets, chest index, pneumonia factors, and the level of tall-like receptor (TLR) signaling pathways in lung tissue.

　　 Results: The levels of CD3 +, CD4 +, CD4 +/CD8 +, chest index and IL-10 in the overexpression group were lower than those in the model group CD8 +, IL-6, TNF-α, TLR2, TLR4, and NF. The -kB level is higher than the model level. (P\u003c0.05). The levels of CD3 +, CD4 +, CD4 +/CD8 +, thoracic index and IL-10 in the silent group were higher than those in the model group, and the levels of CD8 +, IL-6, TNF-α, TLR2, TLR4, and NF-kB were lower than those in the model group ( P\u003c0.05). ). The levels of CD3 +, CD4 +, CD4 +/CD8 +, pleural index and IL-10 in the silent group were higher than those in the overexpression group, while the levels of CD8 +, IL-6, TNF-α, TLR2, TLR4 and NF-kB were lower Overexpression group (P\u003c0.05).

　　 Conclusion: miR-16 silencer can act on the TLR signaling pathway, inhibit the abnormal expression of pathway factors, regulate the body's immune response, and improve the body's immune deficiency, thereby immunizing mice with tuberculosis.