miRNA-16对肺结核模型,免疫功 z-bo 2020-12-09 350

　　Objective To study the regulation and mechanism of silencing miR-16 on the immune function of pulmonary tuberculosis model mice. Methods Forty female CD2F1 mice were selected and divided into normal group, model group, overexpression group, silence group, 10 mice each, model group, overexpression group, and silence group to establish tuberculosis models. After successful modeling, overexpression group and silence group Group mice were injected with 10 μL miR-16 lentivirus suspension aseptically into their lungs. Detect the levels of T lymphocyte subsets, thymus index, lung inflammation factors, and Toll-like receptors (TLRs) signal 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, and the levels of CD8+, IL-6, TNF-α, TLR2, TLR4 and NF-kB were higher than those in the model group (P<0.05). The levels of CD3+, CD4+, CD4+/CD8+, thymus index and IL-10 in the silence 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<0.05 ). The levels of CD3+, CD4+, CD4+/CD8+, thymus index, and IL-10 in the silence group were higher than those in the overexpression group, and the levels of CD8+, IL-6, TNF-α, TLR2, TLR4, and NF-kB were lower than those in the overexpression group (P <0.05).

　　 Conclusion Silencing miR-16 may play a role in regulating the immune function of pulmonary tuberculosis mice by acting on the TLRs signaling pathway, inhibiting the abnormal expression of pathway factors, regulating the body's immune response, and improving the body's immune disorders.