The Effect of Salidroside in the Immune Function of BCG-infected Macrophages

OBJECTIVE To Investigate the affects of salidroside of the immune response of macrophages infected with BCG.METHODS Modelling BCG infection with Raw264.7 mouse macrophages, and the experiments were grouped into blank control group, salidroside(SAL), isoniazid(INH), and salidroside+isoniazid(SAL+INH) groups. The effects of salidroside and isoniazid on the proliferation of Raw264.7 cells were detected by MTT colourimetric assay, and the experimental concentrations of salidroside and isoniazid were screened. After the establishment of BCG-infected macrophage cell model, intracellular bacterial survival was detected by bacterial plate count and flow cytometry after salidroside pretreatment, and the levels of cytokines TNF-α, IFN-γ, IL-6, and IL-10 were detected by ELISA in the supernatants of cell cultures of each group; and apoptosis levels were detected by flow cytometry in the cells of each group.RESULTS SAL was screened to be used at a concentration of 800μM, and INH was used at a concentration of 10μM; compared with the control group, SAL pretreatment for 36 h had the best effect, and the growth of BCG in macrophages in the administered group was inhibited, the inhibitory effect of the combined application of SAL and INH was significant (P<0.05); compared with the control group, in the early stage of the infection, SAL and INH were able to significantly reduce the apoptotic level of BCG-infected Raw264.7 cells in the early stage of infection (P<0.05), but in the late stage of infection, the combination of SAL and INH was able to significantly enhance the apoptosis level of BCG-infected Raw264.7 cells (P<0.05); compared with the control group, SAL reduced but did not significantly differ the levels of TNF-α, IFN-γ, IL-6, and IL-10; however, the combination of SAL combined with INH resulted in a significant reduction in the levels of TNF-α, IL-6 and IL-10 (P<0.05).CONCLUSION SAL can exert their host antimycobacterial effects in BCG-infected macrophages by improving macrophage immune function while attenuating BCG-induced inflammatory responses.