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Objective The aim of this study was to investigate the impact and mechanisms of emodin on oxidative stress response in lipopolysaccharide (LPS)-induced murine mononuclear macrophages (RAW264.7). Methods Involved the use of LPS, RAW264.7 cells, and emodin. Experimental groups included a control group, LPS (1 µg/mL) group, and LPS (1 µg/mL) + emodin (15 µmmol/L) pretreatment group. Aldehyde malondialdehyde (MDA) content, intracellular reactive oxygen species (ROS) levels, and silent information regulator 2 (Sirt2) expression were evaluated at 6, 12, and 18 hours after LPS exposure. Additionally, RAW264.7 cells were pretreated with Sirt2 inhibitor AGK2 (20 «mol/L) followed by LPS stimulation, and the above-mentioned parameters were assessed at 6 hours. Results Compared to the control group, MDA content, ROS levels, Sirt2 mRNA, and protein expression in RAW264.7 cells in the LPS group increased at all time points (all P < 0.05). At 6 and 18 hours, MDA content and ROS levels in RAW264.7 cells in the LPS + emodin group decreased significantly (all P < 0.05), while at 12 hours, ROS levels were lower in the LPS group compared to the LPS + emodin group (P < 0.05). Sirt2 mRNA and protein levels significantly increased at all time points (all P < 0.05) compared to the LPS group. In the LPS + emodin + AGK2 group, Sirt2 mRNA and protein levels decreased, and MDA content and ROS levels increased compared to the LPS + emodin group (all P < 0.05) .Conclusion LPS-induced oxidative stress in RAW264.7 cells and emodin attenuate LPS-induced oxidative stress in RAW264.7 cells through Sirt2. [ABSTRACT FROM AUTHOR]