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目的建立重组人内皮抑素(恩度)联合顺铂一线治疗肿瘤进展的小鼠模型,继续应用内皮抑素联合紫杉醇二线治疗,研究内皮抑素协同紫杉醇抗肿瘤的作用及其机制。方法建立小鼠Lewis肺癌移植瘤动物模型,内皮抑素联合顺铂治疗后观察肿瘤生长情况,遴选出肿瘤进展小鼠16只,随机留取1只,余15只小鼠随机分成紫杉醇组和联合用药组治疗,观察疗效。另取上述肿瘤进展小鼠1只,剥离肿瘤组织,重新接种,将成瘤小鼠随机分成生理盐水组,紫杉醇组及联合用药组治疗,观察疗效。治疗结束后24 h处死所有小鼠,采用免疫组织化学CD31单克隆抗体标记检测微血管密度(MVD),采用原位末端转移酶(TUNEL)检测细胞凋亡。结果 15只肿瘤进展小鼠中,联合用药组相比紫杉醇组生存时间无明显延长,但肿瘤体积增长较慢;而在重新接种成瘤的小鼠中,联合用药组较其余各组微血管密度明显减低(P<0.05),凋亡指数明显增加(P<0.05),肿瘤体积抑制明显。结论在内皮抑素联合顺铂治疗肿瘤进展的小鼠模型中,继续应用内皮抑素治疗与紫杉醇有较明显的协同抗肿瘤作用。
Objective To establish a mouse model of first-line treatment of tumor progression with recombinant human endostatin (Endostar) combined with cisplatin and continue the second-line treatment with endostatin combined with paclitaxel to study the anti-tumor effect of endostatin and paclitaxel and its mechanism. Methods The mouse model of Lewis lung cancer xenografts was established. After the treatment of endostatin combined with cisplatin, the tumor growth was observed. Sixteen mice with tumor progression were selected and one was randomly selected. The remaining 15 mice were randomly divided into paclitaxel group and combination group Treatment group, observe the effect. Another one of the mice with tumor progression mentioned above was stripped of the tumor tissue and re-vaccinated. The tumor-bearing mice were randomly divided into normal saline group, paclitaxel group and combination group, and the curative effect was observed. All mice were sacrificed 24 hours after the end of treatment. Microvessel density (MVD) was detected by immunohistochemistry with CD31 monoclonal antibody, and apoptosis was detected by TUNEL. Results Among the 15 tumor-inducing mice, the combination group showed no significant prolongation of survival time compared with the paclitaxel-treated group, but the tumor volume increased slowly. In the mice re-seeded into the tumor, the combination group showed obvious microvessel density (P <0.05), the apoptosis index increased significantly (P <0.05), and the tumor volume was significantly inhibited. Conclusions Endostatin treatment with paclitaxel has a more obvious synergistic antitumor effect in the mouse model of endostatin and cisplatin in the treatment of tumor progression.