Objective: To investigate intervention of Daotan decoction (DTD) in of intercellular adhesion molecule-1 (ICAM-1) mRNA expression through the regulation of p53 in order to reveal the mechanisms of DTD in the treatment of atherosclerosis. Method: Neonatal umbilical cords were used to isolate endothelial cells

and they were subcultured for 1 to 3 generations in experiment.According to a dose of 0.9 g· kg-1·d-1

DTD was given to SD rats by gavage. Blood samples were obtained via the abdominal aorta after 10 days and the serum was separated. The experiment was divided into 7 groups: blank control group

blank serum control group (HUVECs were treated with serum without DTD)

tumor necrosis factor-α (TNF-α) induced group (200 U· mL-1 TNF-α

12 h)

5% DTD group (5% DTD serum

6 h

and then 200 U· mL-1 TNF-α

12 h)

10% DTD group (10% DTD serum

6 h

and then 200 U· mL-1 TNF-α

12 h)

20% DTD group (20% DTD serum

6 h

and then 200 U· mL-1 TNF-α

12 h) and PFT-α group (p53 blocker) blocking groups (PFT-α 0.009 g· mL-1

30 min

and then 200 U· mL-1 TNF-α

12 h). The impact of DTD on ICAM-1 mRNA and p53 expression in human umbilical vein endothelial cells stimulated by TNF-α were observed with the PCR and Western blot. Result: ①The expression of ICAM-1 mRNA and p53 in the TNF-α induced group was significantly higher than the normal control and DTD control groups. The difference was statistically significant (P<0.01); after being treated with DTD serum or PFT-α

the expressions of ICAM-1 and p53 mRNA were reduced(P<0.05). ②The protein expressions of ICAM-1 and p53 in the TNF-α induced group were significantly higher than the normal control and DTD control groups. The difference was statistically significant (P<0.01); after being treated with DTD serum or PFT-α

the protein expressions of ICAM-1 and p53 were reduced(P<0.05). ③There was a significant positive correlation between the p53 and ICAM-1 mRNA level (r=0.981

P<0.01)

and protein level (r=0.854

P<0.01). Conclusion: DTD inhibits TNF-α stimulation caused ICAM-1 mRNA expression in umbilical vein endothelial cells through the regulation of p53 expression

therefore

it may play a therapeutic role in the treatment of atherosclerosis.