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作 者:孙世宝[1] 盛玉文[1] 于立春[1] 曲更庆[1] 王庆军[1]
机构地区:[1]辽宁医学院附属第一医院泌尿外科,辽宁锦州121001
出 处:《中国药房》2013年第17期1566-1568,共3页China Pharmacy
摘 要:目的:研究体外丝裂霉素(MMC)联合塞来昔布对浅表性膀胱癌T24细胞增殖的影响及其可能机制。方法:体外培养浅表性膀胱癌T24细胞,分为MMC[0(对照组)、2、5、10、25、50μmol/L]组及其与塞来昔布(50μmol/L)混合组,每个浓度5个复孔,采用MTT法检测作用24h后细胞的增殖抑制率。采用免疫组化法、实时定量聚合酶链式反应法、酶联免疫吸附测定法检测对照组、MMC(50μmol/L)组和混合[塞来昔布+MMC(50μmol/L)]组作用48h细胞中Bcl-2蛋白、作用24h细胞血管内皮生长因子(VEGF)mRNA的表达及作用96h内VEGF蛋白浓度。结果:MMC能明显抑制细胞增殖(P<0.05),且呈浓度依赖性;塞来昔布能明显增强MMC对细胞的增殖抑制作用(P<0.05);与对照组比较,MMC组和塞来昔布+MMC组细胞中Bcl-2蛋白、VEGF mRNA表达均明显降低(P<0.05),且后2组组间比较有统计学差异(P<0.05);塞来昔布+MMC组细胞中VEGF蛋白浓度随作用时间延长明显降低(P<0.01)。结论:塞来昔布可协同增强MMC抑制T24细胞增殖的作用,其机制可能与降低Bcl-2、VEGFmRNA表达水平和抑制细胞分泌VEGF蛋白作用有关。OBJECTIVE: To investigate the effects of mitomycin (MMC) combined with celecoxib on the proliferation of superficial bladder cancer cell line T24 and the possible mechanism. METHODS: The superficial bladder cancer T24 cell line were cultured in vitro, and divided into MMC groups [0 (control group), 2, 5, 10, 25 and 50 μmol/L] and MMC combined with celecoxib (50 μmol/L) group with each concentration of 5 bores. MTT method was used to detect the proliferation inhibition rate after 24 h. Immunohistochemistry assay, RT-PCR and ELISA method were adopted to detect the expression of Bcl-2 protein after 48 h of treatment and VEGF mRNA after 24 h of treatment and the protein concentration of VEGF within 96 h of treatment in control group, MMC (50 μmol/L) group and mixture [celecoxib+MMC (50 μmol/L)] group. RESULTS: MMC could inhibit the proliferation of T24 cell (P〈0.05), in dose dependent manner; celecoxib could significantly enhance the inhibitory effect of MMC (P〈 0.05). Compared with control group, the expression of Bcl-2 protein and VEGF mRNA were decreased significantly in MMC group and celecoxib+MMC group (P〈0.05); there was statistical significance between the latter 2 groups (P〈0.05). The concentration of VEGF protein in celecoxib+MMC group was decreased significantly statistically with time (P〈0.01). CONCLUSIONS: Celecoxib can collaboratively enhance inhibitory effect of MMC on the proliferation of T24 cell. The mechanism may be related to reducing the expression of Bcl-2 and VEGF mRNA and inhibiting the secretion of VEGF protein.
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