动物造模,肺结核模型 z-bio 2022-08-26 379

　　Objective To study the regulatory effect and mechanism of silencing miR-16 on immune function in mice with pulmonary tuberculosis.

　　Methods 40 CD2F1 female mice were selected and divided into normal group, model group, overexpression group, and silence group, 10 mice each. Model group, overexpression group, and silence group were used to establish a tuberculosis model. Group mice were aseptically injected with 10 μL of miR-16 lentivirus suspension in the lungs. The levels of T lymphocyte subsets, thymus index, pulmonary inflammatory factors and Toll-like receptors (TLRs) signaling pathway factors in lung tissue were detected.

　　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 disorder.