Artemisinin promotes apoptosis of spinal tuberculosis macrophages by inhibiting NF-κB

Abstract

Artemisinin has been proved to have a wide range of pharmacological effects, mainly used in anti-malaria, anti-inflammatory, antiviral, etc., but the effect and mechanism of artemisinin on tuberculosis-infected macrophages have not yet been elucidated. THP-1 cell line was cultured and randomly divided into the following 4 groups; control group, which was infected with Mtb standard human virulence strain H37Rv; low-dose, medium-dose and high-dose artemisinin groups, which were treated with artemisinin at 50 μM, 150 μM and 300 μM, respectively. The effect of artemisinin on cell proliferation was determined by MTT assay. MMP-2 and MMP-9 were detected by PCR. The inflammatory cytokines IL-6 and TNF-α were detected by ELISA. The above tests were used to understand apoptosis, inflammation and proliferation. The expressions of Bcl-2, osteoprotectin (OPG), nuclear factor κB receptor activator (RANK) and NF-κB were detected by Western blot. Acting on macrophages infected with mycobacterium tuberculosis, artemisinin can significantly inhibit cell proliferation, promote cell apoptosis, inhibit the expression of MMP-2 and MMP-9, and reduce the secretion of IL-6 and TNF-α. Artemisinin also decreased the expression of Bcl-2, OPG, RANK and NF-κB (p < 0.05), and the change was more significant with the increase of dose. Artemisinin could down-regulate the expression of OPG, RANK and NF-κB, and inhibiting the expression of inflammatory factors and Matrix metalloproteinases (MMPs), and then promoting apoptosis of spinal tuberculosis macrophages.