Vitamin C inhibits apoptosis in THP‑1 cells in response to incubation with <i>Mycobacterium tuberculosis</i>

Tuberculosis (TB) is a chronic and fatal zoonotic infectious disease caused by <em>Mycobacterium tuberculosis</em> (<em>M. tb</em>) 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 <em>M. tb</em>. Macrophages are important for the progression of tuberculosis, as they affect the release of various inflammatory cytokines, including IL‑1β, 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 <em>M. tb</em> 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 <em>M. tb</em> following vitamin C treatment. The effect of vitamin C on <em>M. tb</em> infection was also assessed using Balb/c mice; pulmonary injury was assessed by H&amp;E staining of the lung tissue. The results demonstrated that vitamin C markedly attenuated cellular damage caused by <em>M. tb</em> infection. The results demonstrated that vitamin C reduced the expression of <em>M. tb</em>‑induced apoptosis‑related proteins (Cleaved‑caspase‑9, Cleaved‑caspase‑3, Bcl‑2, Cyt‑c) and inflammatory factors (IL‑1β, 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 <em>M. tb</em> infection.