动物造模,肺结核模型 z-bio 2021-08-10 760

　　Objective: To study the regulatory effect 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 and silent group, each with 10 mice, model group, overexpression group and silent group. After successful modeling of tuberculosis model, 10 μL The miR-16 lentiviral suspension was injected into overexpressed silent mice and injected aseptically into the lungs. Detect the levels of T lymphocyte subsets, thymus index, pulmonary inflammatory factors and Toll-like receptor (TLR) signaling pathway factors in lung tissue.

　　Results: The levels of CD3+, CD4+, CD4+/CD8+, thymus index, and IL-10 in the overexpression group were lower than those in the model group, but CD8+, IL-6, TNF-α, TLR2, TLR4, and NF-kB were all higher than those in the model group (Pu003c0 .05). The levels of CD3+, CD4+, CD4+/CD8+, thymus index, and IL-10 in the silent group were higher than those in the model group, and CD8+, IL-6, TNF-α, TLR2, TLR4, and NF-kB were lower than the model group (Pu003c0.05). The levels of CD3+, CD4+, CD4+/CD8+, thymus index, and IL-10 in the silence group were higher than those in the overexpression group. CD8+, IL-6, TNF-α, TLR2, TLR4, and NF-kB were all lower than the overexpression group (Pu003c0. 05).

　　Conclusion: miR-16 silencer acts on the TLR signaling pathway, inhibits the abnormal expression of pathway factors, regulates the body's immune response, improves the body's immune deficiency, and thereby immunizes tuberculosis mice, which may play a regulatory role.