Aim To investigate the effect of ligustrazine (LIG) on inflammatory injury induced by lipopolysaccharide (LPS) in human coronary artery endothelial cells (HCAEC) and explore its possible mechanism. Methods After pretreatment with LIG (1,0, 100 μmol/L) for 12 hours, HCAEC cells were co-treated by LPS (1 mg/L) and LIG for 24 hours. Cell viability was tested by methyl thiazolyl tetrazolium (MTT) assay. Apoptosis rate of HCAEC was detected by flow cytometry. Levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in supernatant of cell culture medium were tested by enzyme linked immunosorbent assay (ELISA). Expression of ATP-binding cassette transporter A1 (ABCA1) protein in HCAEC cells were measured by Western blot. Results Compared with control group, the cell viability of HCAEC was significantly decreased, the apoptosis rate of HCAEC was significantly increased, the levels of IL-6 and TNF-α in supernatant of cell culture medium were significantly increased, expression of ABCA1 protein in HCAEC was significantly down-regulated in LPS group (all P＜0.05). Compared with LPS group, the cell viability of HCAEC was significantly increased, the apoptosis rate of HCAEC was significantly decreased, the levels of IL-6 and TNF-α in supernatant of cell culture medium were significantly decreased, expression of ABCA1 protein in HCAEC were significantly up-regulated in LIG (10 and 100 μmol/L)＋LPS group (all P＜0.05). Conclusion LIG inhibits the inflammatory injury induced by LPS in HCAECs, and its mechanism may be related to LIG up-regulating the expression of ABCA1.