| Objective:Benign prosatic hyperplasia(BPH) is a common disease in aged male.The pathogenesis of the disease is still not very clear until now.We only know that it is an androgen-dependent and age-related disease。In all of the theories about the pathogenesis of BPH, people is paying increasing attention to the peptide growth factor theory.Study on the growth factors which mediate stromal-epithelial interaction is more than before.And many growth factors have been detected in BPH.Up to nowdays,study on the function of growth facors in BPH mainly focus on the direct regulation activity on prostate stromal and epithelial cells ,such as growth,proliferation,apoptosis.While many of them can mediate angiogenesis,such as basic fibroblast growth factor (bFGF), vascular endothelial growth factor(VEGF),platelet derived growth factor(PDGF),transforming growth factorβ( TGF-β),epidermal growh factor(EGF),et al.They directly or undirectly regulate angiogenesis via different receptor.But it is unclear whether this kind of function play a role on the pathogenesis of BPH.And study on the angiogenesis in BPH is very little. Angiogenesis is that on the basis of capillary blood vessels or microvein , through vascular endothelia cell proliferating,migrating,new capillary blood vessels are formed from subsistent vessels by the way of budding or unbudding.It is the primary mode of vessel formation during embryo shaping and normal tissue building post partum..It also is mostly mode of vessel formation and increasing during pathological tissue development.The increasing of angiogenesis closely involved in the development of benign and malignant tomour.Angiogenesis is decided by two reason .One is the increasing of angiogenesis promotors,the other is the decreasing of angiogenesis inhibitors.Study on angiogennesis inhibitors of BPH tissue is also very little.Thrombospondin-1(TSP-1),as a important angiogenesis inhibitor in vivo,is gradually noticed by people in recent year.It plays an important role in inhibiting proliferation, migration and inducing apoptosis of endothelia cell,being a physiological angiogenesis inhibitor.Study on the relation of TSP-1 and BPH is not much and none at home..By studying the expression of angiogenesis promotor bFGF and inhibitor TSP-1 in normal prostate and benign hyperplasic ,also detecting microvessel density (MVD) in both tissues,we explored the effect of angiogenesis during pathogenesis of BPH.Methods:Specimens were obtained from human prostate and divided into two groups:(1)hyperplastic prostate group:The specimens were removed from BPH patients by suprapubic prostatectomy(n=30, 58-78 years old,mean 68.2years old).Tissues were immediately cut into 3-5mm thick sections from specimens and immerged into 10%folmalin after the specimens were removed from body,and then stored at 4℃.all of specimens were proved to be BPH tissue b by microscopic observation of HE tissue dyeing.(2)normal prostate group:The normal specimens were obtained from corpses(n=10, 21-30 years old,mean 25.4years old ) The tissues taking and storage were same with BPH group.All of specimens were proved by microscopic observation of HE tissue dyeing.The specimens were made paraffin-embedded formalin-fixed tissue sections. The sections were subjected to microwarve antigen retrieval and stained for TSP-1,bFGF using immunohistochemistry.Tissue sections were immunostained for microvessel density with a CD34 antibody and a microwave antigen retrieval step.Microvessel density was calculated by counting CD34 positive endothelial-lined vessels in five non-overlapping random high poeer fields (40×) within intratumoral regions.Result:(1)TSP-1 localized mainly to the epithelium and moderately to the stroma in norm- al prostate tissue.The staining of TSP-1decreased when normal tissue was compared to BPH (P＜0.05).(2)The staining of bFGF localized mostly in the stroma and minimal in the epithelium.And showed a stepwise increase when BPH tissue was compared with normal prostate tissue .(P＜0.05) (3) Microvessel density i... |
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