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作 者:李华菊[1] 陈红[1] 曾委[1] 潘虹[1] 邹阳[1] 段洁[1] 左帆[1]
机构地区:[1]武汉大学中南医院妇产科,湖北武汉430071
出 处:《武汉大学学报(医学版)》2013年第5期695-698,共4页Medical Journal of Wuhan University
摘 要:目的:研究米非司酮(MIF)裸鼠体内逆转人宫颈癌Hela/MMC细胞系对丝裂霉素(MMC)耐药的效果及其作用机制。方法:以人宫颈癌Hela细胞耐药亚系(Hela/MMC细胞)为材料,建立裸鼠移植瘤模型,随机分为4组:空白对照组、单用MIF组、单用MMC组、联合用药组,观察用药后移植瘤的体积、瘤重及裸鼠体重,光镜下观察瘤组织病理学改变及裸鼠主要脏器的病理情况,免疫组织化学染色法检测移植瘤增殖细胞相关核抗原ki-67的表达。结果:联合用药组平均瘤体积(288.61±93.70)mm3较对照组(998.93±219.10)mm3及单用MIF组(903.01±288.51)mm3显著降低(P<0.01),较MMC组(693.33±230.75)mm3明显降低(P<0.05);联合用药组平均瘤重(0.14±0.04)g较对照组(0.41±0.07)g、单用MIF组(0.37±0.10)g及单用MMC组(0.32±0.08)g明显降低,差异有显著性(P<0.01);联用组ki-67表达的平均光密度值(OD)(0.21±0.01)较对照组(0.56±0.04)、单用MIF组(0.37±0.02)及单用MMC组(0.55±0.04)明显降低,差异有显著性(P<0.01);单用MIF组平均光密度值较对照组及单用MMC组显著降低(P<0.01),对照组与单用MMC组比较,差异无显著性(P>0.05)。联合用药组肿瘤形态出现明显坏死,各组裸鼠体重无显著性差异(P>0.05),裸鼠主要脏器无明显病理变化。结论:米非司酮裸鼠体内可逆转Hela/MMC细胞对MMC的耐药性且无明显毒副作用,其逆转耐药机制可能与降低增殖细胞相关核抗原(ki-67)的表达有关。Objective. To study the reversal effect of mifepristone on the MMC-resistant human cervical cancer cell subline in vivo and its mechanism. Methods. The nude mice xenografted tumor mod- els were established by transplantating the MMC-resistant human cervical cancer cell subline to nude mice. When the models were established, the nude mice were randomly divided into con- trol, mifepristone, mitomycin and mifepristoneff-mitomycin groups. The xenografted implants volumes were figured up and the growth curve was mapped. The nude mice were sacrificed 3 days after the last administration, and every xenografted implant was obtained and weighed. The changes of morphology xenofraft tissue were observed by light microscopy with HE staining. The expression ki-67 in xenograft tissue was investigated by the immunohistoehemistry. Resuits Thexenografted implants' volume, weight, ki-67 expression in mifepristone mitomycin group was respectively less than that respectively in control group, and mifepristone group, mitomycin group (P〈O. O1 or P%0.05). Mifepristone Mitomycin group appeared a typical morphology changes, necrosis. Conclusion: Mifepristone has reversal effect on the MMC-resistant human cer- vical cancer cell subline in vivo without obvious side-effect, and its mechanism may be relevant with the decrease of the expression of ki-67.
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