Vitamin C inhibits apoptosis in THP­1 cells in response to incubation with Mycobacterium tuberculosis.

Tuberculosis (TB) is a chronic and fatal zoonotic infectious disease caused by Mycobacterium tuberculosis (M. tb) infection. The THP-1 cell line is a cell model for studying the function, mechanism and signaling pathways of macrophages; macrophages are the primary host cells of M. tb. Macrophages are important for the progression of tuberculosis, as they affect the release of various inflammatory cytokines, including IL-1ß, IL-6 and TNF-α. Vitamin C is a trace element for the human body. Its biological efficacy depends on its redox abilities and its role as a cofactor in several enzymatic reactions. However, whether vitamin C can protect THP-1 cells from M. tb infection has not yet been reported. The present study aimed to further investigate the effects of vitamin C on M. tb infection-induced THP-1 cell injury and its mechanism. In the present study, MTT assay, reverse transcription-quantitative PCR, EdU cell proliferation assay, western blotting, immunohistochemistry, flow cytometry and TUNEL staining assays were used to assess the cell viability, inflammation and apoptotic levels of THP-1 cells induced by M. tb following vitamin C treatment. The effect of vitamin C on M. tb infection was also assessed using Balb/c mice; pulmonary injury was assessed by H&E staining of the lung tissue. The results demonstrated that vitamin C markedly attenuated cellular damage caused by M. tb infection. The results demonstrated that vitamin C reduced the expression of M. tb-induced apoptosis-related proteins (Cleaved-caspase-9, Cleaved-caspase-3, Bcl-2, Cyt-c) and inflammatory factors (IL-1ß, IL-6, NLRP3, TNF-α, IL-8, NF-κB) in THP-1 cells and reduced apoptosis. Overall, these results suggested that vitamin C may reduce lung damage caused by M. tb infection.