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作 者:李国灏[1] 李运柱[1] 李文洲[1] 陈琳[1] 胡卫锋[1]
出 处:《临床泌尿外科杂志》2011年第3期224-227,230,共5页Journal of Clinical Urology
基 金:武汉市卫生局资助项目(编号WX09D01)
摘 要:探讨血管紧张素Ⅱ,型受体(ATIR)拮抗剂坎地沙坦对膀胱癌BIU-87细胞株的生物学行为的影响。方法:采用免疫组织化学SABC法检测膀胱癌BIU-87细胞株ATIR的表达,用MMT法检测用坎地沙坦处理后的BIU 87细胞株的生长情况,同时检测BIU-87细胞株的侵袭能力和黏附能力,用ELISA法检测血管内皮细胞生长因子和白细胞介素-8的表达水平。结果:ATIR拮抗剂坎地沙坦不影响BIU-87细胞株的生长,但能降低其侵袭能力和黏附能力,也能抑制血管内皮细胞生长因子和白细胞介素-8的表达。结论:ATIR拮抗剂通过降低肿瘤细胞的侵袭黏附能力和抑制血管生成而达到抗癌作用,AT、IR拮抗剂将来可能会成为一种抗癌治疗的新方法。To investigate the effect of ATIR antagonist(candesartan) on the biological behavior of bladder cancer cell lines(BIU-87). Methods: Immunochemical SABC method was used to detect the expression of AT1R in bladder cancer cell lines(BIU-87), MMT method was used to detect the growth of the BIU-87 cells treated by candesartan,the invasiveness and the adhersion of the BIU-87 cells were analyzed, the expression of VEGF and IL-8 were assessed by EI.ISA. Results.. Candesartan did not effect the growth of BIU-87 cells,but the invasiveness and tile adhersion of the BIU-87 ceils were lower than the control group,the expression of VEGF and IL-8 were decreased by candesartan. Conclusions: AT1R antagonist prevented bladder tumor growth by inhibiting the the invasiver-ess and the adhersion of BIU-87 cells and angiogenesis,and it is possible for AT1R antagonist to be the new approach of anticancer therapy.
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