目的:检测质膜微囊结构蛋白caveolin-2在内皮-单核细胞激活多肽-II(EMAP—II)增强血肿瘤屏障(BTB)通透性过程中的表达水平变化。方法:荷瘤Wistar大鼠被随机分成4组(每组16只):EMAP—II处理0h、1h、2h和4h组。采用伊文思蓝渗透性实验评估各组BTB通透性变化情况;RT—PCR、Westernblot.ting、免疫组化和免疫荧光法检测脑胶质瘤组织毛细血管上caveolin-2的表达水平变化。结果:EMAP—II作用1h时,BTB的通透性显著增强,随后逐渐降低,4h时恢复正常;同时,EMAP—II作用1h时,脑胶质瘤组织毛细血管上caveolin-2的表达水平显著增高,随后逐渐降低,4h时恢复正常。结论:EMAP—II可能通过cayeolae介导的跨细胞途径来增强BTB的通透性,其机制与caveolin-2的表达水平上调有关。
Objective: To detect changes in the expression level of caveolar structural protein caveolin - 2 in endo- thelial monocyte activating polypeptide- II( EMAP -II ) -induced increase in blood -tumor barrier( BTB )permea- bility. Methods:Tumor- bearing rats were randomly divided into 4 groups( n = 16, each) : EMAP- II Oh, l h ,2h and 4h groups. Evans blue method was used to evaluate the alterations in BTB permeability. Changes in the expression lev- el of the caveolar structural protein caveolin - 2 in brain capillaries were measured by RT - PCR, Western blotting, immunohistochemistry and immunofluorescent assays. Results:The EB content in tumor tissues increased significantly at 1 h after EMAP - II administration, and trended back toward the level of the EMAP - II Oh group gradually by 4h. The expression levels of caveolin -2 in brain capillaries were significantly increased at lh, and decreased gradually toward the untreated level thereafter. Conclusion: EMAP - II may induce BTB hyperpermeability via caveolae - medi- ated transcellular pathway, which is associated with the upregulation of caveolin - 2.