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In this study, mammary epithelial cells (MAC-T) cells were used as models to investigate the effects of Lipopolysaccharides (LPS) on oxidative stress, inflammation, autophagy, and apoptosis, as well as the role of the AMPK/mTOR/ULK1 pathway in LPS-induced inflammatory damage. CCK-8 and lactate dehydrogenase (LDH) assays were used to detect MAC-T cell activity. Hoechst 33342 stained and evaluated the nuclear morphology of MAC-T cells. Real-time quantitative PCR and western blotting were used to detect the expression levels of genes and proteins related to autophagy, apoptosis, inflammation, and oxidative stress, respectively. The results showed that LPS inhibited the proliferation of MAC-T cells, upregulated the expression of inflammatory factors, increased oxidative stress levels, activated autophagy, and induced apoptosis. The AMPK/mTOR/ULK1 pathway was involved in the regulation of LPS-induced autophagy and apoptosis of MAC-T cells. Conclusion LPS regulates autophagy and apoptosis of MAC-T cells through the AMPK/mTOR/ULK1 pathway. Increased autophagy in MAC-T cells blocks the flow of autophagy, thereby promoting apoptosis.