Mcl-1 signals pathway inhibitors in mouse peritoneal macrophage apoptosis infected with the Xinjiang strain of

A present, myeloid cell leukemia-1 (Mcl-1) was suggested as a potential new target for controlling latent TB infection. Therefore, we investigated the role of the Mcl-1 signalling pathway in mouse peritoneal macrophages infected with XJ-MTB, aiming at finding a new strategy for TB management in Xinjiang. We using TUNEL, Immunohistochemical analysis, ELISA, HE, RT-PCR and Western blot detected macrophages apoptosis, the damage of mice tissues and the expression of apoptosis genes and proteins. Results found that inhibition of the Mcl-1 signalling pathway not only reduced the survival of intracellular XJ-MTB, but also increased peritoneal macrophage apoptosis in latent XJ-MTB-infected mouse peritoneal macrophages and relieved the pathological damage of mouse organs infected with XJ-MTB, especially MAPK signalling pathway inhibitor PD98059 (P<0.05). Moreover, after inhibitor PD98059 treated mouse peritoneal macrophages infected with XJ-MTB, Bcl-2, Bax and Mcl-1 were reduced, while Cytochrome-c and Caspase-8 protein levels were significantly increased, and Cytochrome-c protein levels was significant higher than Caspase-8 (P<0.05). In conclusion, the MAPK signalling pathway inhibitor PD98059 down-regulated Mcl-1 expression and effectively increased macrophage apoptosis in mice infected with XJ-MTB. Furthermore, it also relief pathological organ damage and promote the elimination of inflammation. The intrinsic apoptotic pathway plays a predominant role in the regulatory role.