Objective: To observe the effect of intralesional administration of triamcinolone acetonide on the graft hemangioma in nude mouse and to explore the mechanism of glucocorticoid intervention.
Methods: The specimen of proliferating hemangioma from a male infant of 2 months old was obtained by surgery. The tissue was cut into small pieces 5 mm x 4 mm x 3 mm in size and grafted onto nude mice subcutaneously. Triamcinolone acetonide was administered intralesionally at 45th day after graft. Grafted specimens were taken before and at 3rd day, 1st week, and 2nd week after triamcinolone acetonide administration. In mice of control group, introlesional injection of the same volume of normal saline was given. Glucocorticoid receptor (GR), Vascular endothelial growth factor (VEGF) and Ki-67 were detected.
Results: Significant decrease of graft volume was observed in the experimental group compared to that in control group, and the grafts in experimental group turned harden and whitish in 2 weeks. Under microscopy, grafts of experimental group were mainly composed of lipofibrous tissue. Collapse and blockage of vascular lumens were frequent. While control grafts involved large amount of proliferative capillaries and signs of destruction was not observed. With administration of triamcinolone acetonide injection, the stainings of GR, VEGF, and Ki-67 turned weaker significantly. Significant differences of GR, VEGF, and Ki-67 staining were obtained between experimental group and control group, and between experimental group and normal subcutaneous tissue group. After intralesional administration of triamcinolone acetonide, the coefficient correlations of GR to VEGF and to Ki-67 were 0.766 (P < 0.01) and 0.643 (P < 0.01), respectively. The coeffecient correlation of VEGF to Ki-67 was 0.567 (P < 0.05).
Conclusion: The effect of external glucocorticoid on hemangioma might be mediated by GR, i.e., glucocorticoid binds to it is specific receptor and forms a glucocorticoid-GR complex, and the complex interacts with glucocorticoid response element in target gene, and then inhibit secretion of VEGF. With decreased VEGF secretion, proliferation of endothelial cells is hampered and the hemangioma involutes.