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Melatonin administration reversed this phenotype by adopting a compensatory mechanism aimed at increasing Bcl-2 protein expression, blocking Bax proapoptotic activity via the SIRT1/NF-kB axis with a consequent and significant inhibition of Cyt C release and the lack of apoptosome formation and caspase 3 activation 37 (Fig

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2006;136(6 Suppl):1636S40S

demonstrated that blocking vascular endothelial growth factor (VEGF) signaling with antibodies against VEGF or VEGFR-2 reduced M.tb transmission to the lung, spleen, and liver in M.tb -infected mice [112]

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