Objective To investigate the regulatory role of the clinical hepatinica, polyene phosphatidylcholine(PPC), on LPS-induced macrophage inflammatory response and whether phosphate and tension homology deleted onchromosome ten (PTEN) is involved in the process. The study also preliminarily determined the anti-inflammatory effect ofPPC and its underlying mechanisms. Methods Raw 264. 7 cells were inoculated on cell culture plates and divided into sixgroups, which were labeled and induced as follows: PPC (20 μg/ mL), LPS (100 ng/ mL), LPS (100 ng/ mL) + PPC(20 μg/ mL), PPC (20 μg/ mL) + SF1670 (150 ng/ mL), PPC (20 μg/ mL) + SF1670 (150 ng/ mL) + LPS (100 ng/mL) or an equal volume of phosphate-buffered saline (PBS) groups. The cells and supernatants were collected after 24 h.Enzyme-linked immunosorbent assay was used to detect the levels of IL-6, IL-10 and TNF-α. RT-PCR was applied to detectthe mRNA expression of IL-6. Western blot was performed to confirm the PTEN protein expression. Results TNF-α andIL-10 levels in the supernatants did not significantly differ between the PBS and PPC groups. Compared with the LPSgroup, the TNF-α and IL-6 levels in culture supernatants of the PPC+LPS group decreased significantly ( P <0. 001),while the IL-10 level increased significantly ( P <0. 001). PTEN protein expression in the PPC+LPS group was significantlyhigher than that of the LPS group. Compared with the PPC group, the TNF-α levels and IL-6 mRNA expression in the PPC+SF1670 group were significantly increased ( P <0. 05). The PPC+LPS+SF1670 group showed elevated TNF-α and IL-6production ( P <0. 001) but lower IL-10 production ( P <0. 001) than that of the PPC+LPS group. Conclusions PPC inhibits LPS-induced macrophage inflammatory response by upregulating PTEN expression.