Abstract: Objective: To investigate the regulator role of Bcl-2 family proteins on the apoptosis of mouse Raw264.7 macrophages infected with different virulent of M. tuberculosis strains whentarget Mcl-1 expression by using RNA interference. Methods: Raw264.7 macrophages were infected by XJ-MTB, H37Rv, H37Raand BCG strains, Mcl-1shRNA was treated the infection cells. The apoptosis rate of macrophages was detected by flow cytometry. The expressions of Mcl-1 and Bax protein were detected by Western blot. The expression of Bcl-2 family genes and the expression of Caspase-3 and Cytochrome-c were detected by Real-time PCR. Results: 1) Infection with different virulence of M. tuberculosis induced mouse Raw264.7 macrophages apoptosis, down-regulate Mcl-1 could significantly increase the apoptosis rate of host macrophages infected with XJ-MTB and H37Rv. 2) Infection with XJ-MTB and H37Rv could significantly up-regulate the expression of Mcl-1 and Bcl-2 in host macrophages, the levels of Mcl-1 and Bcl-2 were significantly decreased after silencing Mcl-1 expression, while increasing the expression of Bax. 3) M. tuberculosis infection could induce host macrophages Caspase-3 and Cytochrome-c expression, down-regulation of Mcl-1 could up-regulate the expression of Caspase-3 and Cytochrome-c in host. Conclusion: The expression of Bcl-2 family members in host macrophages induced by M. tuberculosis infection associated with the virulence of M. tuberculosis. Down-regulate Mcl-1 expression by Mcl-1 shRNA could promote host macrophages apoptosis.

Key words: Bcl-2 family members, Mcl-1, MTB, apoptosis