Aim To study the mechanism of anti-injury of pariphyllin on the human umbiliar vein endothelial cell (hUVEC) ECV 304 induced by hydrogen peroxide (H2O2). Methods A model of endothelial cell oxidative damage induced into H2O2 was established, then cells were divided into five experimental groups including normal group, oxidative damage group and three different concertration pariphyllin groups. MTT assay was used to detect the protection of pariphyllin, reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the mRNA expression level of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), flow cytometry (FCM) was used to quantitate the expression of ICAM-1 and VCAM-1. Results Cell optical density in oxidation damaged group was lower than nomal control (P<0.01); when pretreated by the medicine, the OD value was increased, and it had no significant difference in the high density pariphyllin than normal control (P>0.05). The mRNA expression of ICAM-1and VCAM-1 was significantly descended (P<0.01) in medicine treatment groups than in H2O2 damage group, FCM result discovered that the numbers of masculine cells which express ICAM-1 or VCAM-1 were obviously more than other groups (P<0.01), but pretreated group could make the number lower and the effection was dose dependent. Conclusions Pariphyllin has the protective action on oxidative damage of ECV304, which was related to stabilizing the cell wall to inhibit the inflammatory reaction induced by ICAM-1 and VCAM-1, and then protect endothelial cell, prevent atherosclerosis.