Objective: To observe the antitumor and anti-angiogenesis effect of ellagic acid against the transplantation tumor of S180 and H22 in mice

and to explore its possible mechanism by investigating the protein expressions of platelet-derived growth factor-B (PDGFB)

signal transducer and activator of transcription-3 (STAT3) and p-STAT3 in vivo. Method: Mice bearing S180 and H22 cells were randomly divided into 5 groups:the model group (5% CMC)

the cyclophosphamide group (20 μg·g-1·d-1)

the high-

middle- and low-dose ellagic acid groups (200

100

50 μg·g-1·d-1). The mice were administrated with corresponding medicines for successive 10 days. The tumor inhibitory ratios

body weight

the thymus and spleen index were measured

respectively. The effect on microvascular density

PDGFB

p-STAT3 and STAT3 expressions were detected by using an immunohistochemicalassay assay. Result: The tumor inhibitory ratios of the high-

middle- and low-dose ellagic acid were 35.3%

10.6% and 5.6% on S180-bearing mice

and 36.3%

38.8%

20.6% on H22-bearing mice. While

no significant influence on the body weight was found. Compared with the model group

the spleen index was higher in the high- dose group (P<0.05)

and the microvascular density were lower in the high-and middle-dose groups (P<0.05)

the expressions of PDGFB

p-STAT3 and STAT3 were lower in all doses of ellagic acid groups. Conclusion: Ellagic acid could inhibit the tumor growth and angiogenesis against the transplantation tumor of S180

H22 effectively. Its mechanism may be related to decreasing expression of PDGFB and further the expression and the phosphorylation of STAT3.