To determine the effect of NF-kappa B on cell proliferation and apoptosis, we investigate the expression of inflammation and apoptosis-related factors in the bovine mammary epithelial cell line, MAC-T. MAC-T cells were cultured in vitro and MTT and LDH assays used to determine the effects of lipopolysaccharide (LPS) on proliferation and cytotoxicity respectively. RT-PCR and western blotting were used to evaluate the effect of LPS and NF-kappa B inhibition [pyrrolidine dithiocarbamate (PDTC) treatment] on the expression of inflammation and apoptosis-related factors. LPS significantly inhibited MAC-T cell proliferation in a dose- and time-dependent manner. Furthermore, LPS promoted apoptosis while the NF-(DB)-B-0 inhibitor PDTC attenuated this effect. After LPS treatment, the NF-(DB)-B-0 signaling pathway was activated, and the expression of inflammation and apoptosis-related factors increased. When PDTC blocked NF-(DB)-B-0 signaling, the expression of inflammation and apoptosis-related factors were decreased in MAC-T cells. LPS activates the TLR4/NF-kappa B signaling pathway, inhibits proliferation and promotes apoptosis in MAC-T cells. NF-(DB)-B-0 inhibition attenuates MAC-T cell apoptosis and TLR4/NF-kappa B signaling pathway. NF-(DB)-B-0 inhibitor alleviating MAC-T cell apoptosis is presumably modulated by NF-(DB)-B-0.