动物造模,肺结核模型 z-bio 2022-11-02 297

　　Objective To study the regulatory effect of silent miR-16 on immune function of pulmonary tuberculosis model mice and its mechanism.

　　Methods Forty CD2F1 female mice were selected and divided into normal group, model group, overexpression group and silence group, 10 mice in each group. The model group, overexpression group and silence group were used to establish the pulmonary tuberculosis model. After successful modeling, the mice in overexpression group and silence group were injected 10 μ L miR-16 lentivirus suspension. The levels of T lymphocyte subsets, thymus index, pulmonary inflammatory factors and Toll like receptors (TLRs) signal pathway factors in lung tissues 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- α、 The levels of TLR2, TLR4 and NF kB in the model group were higher than those in the model group (P<0.05). The levels of CD3+, CD4+, CD4+/CD8+, thymus index and IL-10 in mice in the silent group were higher than those in the model group- α、 The levels of TLR2, TLR4 and NF kB in the model group were lower than those in the model group (P<0.05). The levels of CD3+, CD4+, CD4+/CD8+, thymus index, IL-10 in mice in the silence group were higher than those in the overexpression group, CD8+, IL-6, TNF- α、 The levels of TLR2, TLR4 and NF kB in the overexpression group 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 TLRs signal pathway, inhibiting the abnormal expression of pathway factors, regulating the immune response of the body, and improving the immune disorder of the body.