Background: Psoriasis is a chronic inflammatory skin disorder of unknown etiology. Increasing
evidence suggests that psoriasis is probably an angiogenesis-dependent disease. Thalidomide has
been reported being able to inhibit the effects of fibroblast growth factor 2 and vascular endothelial
growth factor (VEGF), and inhibit tumour necrosis factor-alpha synthesis, and suppress tumour necrosis
factor-induced nuclear factor-kappa B activation in Jurkat cells, resulting in suppression of proliferation
inflammation, angiogenesis, and the immune system, which are related to the pathogenesis of psoriasis.
Objective: Our study evaluated the influence of thalidomide on the lesional alterations, VEGF expressions
and angiogenesis in imiquimod-induced mouse model.
Methods: Balb/c female mice (n=48) 8-12 weeks of age were randomly divided into 6 groups including
negative control (vaseline cream), positive control (5% imiquimod cream), and experimental groups
including low-dose (10 mg/kg.d), moderate-dose (30 mg/kg.d) and high-dose thalidomide (85 mg/kg.d),
and acitretin group (6 mg/kg.d). Serum levels of VEGF-A were quantified by enzyme-linked immunosorbent
assay. VEGF protein expression was measured by western blotting and the microvessel density
by immunohistochemical staining.
Results: The total psoriasis area and severity index scores in the moderate- and high-dose thalidomide
and acitretin groups decreased significantly (p<0.001 for each), and so were the total Baker’s scores in
the high-dose thalidomide (p=0.008) and acitretin groups (p=0.021). The mean thickness of the epidermis
in the experimental and acitretin groups decreased significantly, respectively (p<0.001 for all); the
acitretin group was the thinnest. The cutaneous VEGF protein levels down-expressed significantly in the
moderate- and high-dose thalidomide groups (p<0.05 for both), while those in the low-dose thalidomide
and acitretin did not (p>0.05 for both). There were no differences for serum VEGF-A levels and the
density of microvessels among the positive and experimental groups.
Conclusion: Thalidomide can improve the psoriasis-like lesions and inhibit the expression of cutaneous
VEGF in imiquimod-induced psoriatic model with dose-dependence, however, it does not alter circulating
VEGF-A levels and microvessel density in dermis.