Abstract: Objective: To observe the protective effect of procyanidin B1 (PB1) on the lipopolysaccharide (LPS)-induced injury of macrophages RAW264.7, and to explore its possible mechanism. Methods: The macrophages RAW264.7 in logarithmic phase cultured in vitro were divided into control group (without treatment), LPS group (treated with 2 mg·L^-1 LPS), PB1 group (treated with 10 μmol·L^-1 PB1) and PB1 + LPS group (treated with 2 mg·L^-1 LPS and 10 μmol·L^-1 PB1). The morphology of cells was observed under microscope, the levels of reactive oxygen species (ROS) in the cells,the apoptotic rates of the cells and the expression levels of CD16/32, CD40, CD86, and Toll-like receptor 4(TLR4) on cell surface of the cells in various groups were detected by flow cytometry. Results: Compared with control group, the cells in LPS group were shrunk and round,but the morphological changes of the cells in PB1 group and PB1 + LPS group were not significant. Compared with control group, the ROS level in the cells in LPS group was significantly increased (P<0.05); compared with LPS group, the ROS level in the cells in PB1 + LPS group was significantly decreased (P<0.05). Compared with control group, the apoptotic rate of the cells in LPS group was decreased (P<0.05); compared with LPS group, the apoptotic rate of the cells in PB1 + LPS group was increased(P<0.05). Compared with control group, the expression levels of cell surface molecules CD16/32, CD40, CD86, and TLR4 in the cells in LPS group were increased (P<0.05); compared with LPS group, the expression levels of cell surface molecules CD16/32, CD40, CD86, and TLR4 in the cells in PB1 + LPS group were decreased (P<0.05). Conclusion: LPS can induce the cell injury by increasing the ROS level, and PB1 can protect the cells by decreasing the ROS level and down-regulating the expression levels of cell surface molecules CD16/32, CD40, CD86, and TLR4.

Key words: procyanidin B1, macrophages, lipopolysaccharide, damage, apoptosis