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肺抑瘤膏联合吉非替尼对Lewis荷瘤小鼠模型的抗肿瘤血管生成作用研究 被引量:9

Inhibition of FeiYiLiuGao combined with gefitinib on lewis lung carcinoma in mice: impressive modifications of serum levels of angiogenic-related factors
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摘要 目的研究肺抑瘤膏联合吉非替尼对非小细胞型肺癌(NSCLC)的抗肿瘤血管生成作用。方法本实验建立Lewis肺癌(LLC)荷瘤小鼠模型,随机分为4组。对照组给予生理盐水,肺抑瘤膏组给予肺抑瘤膏治疗,吉非替尼组给予吉非替尼治疗,肺抑瘤膏联合吉非替尼组给予肺抑瘤膏和吉非替尼治疗,疗程14 d。观察肺抑瘤膏联合吉非替尼的抗肿瘤作用,称瘤重、计算抑瘤率,通过ELISA方法检测血管生成促进性因子血管内皮生长因子(VEGF)和抑制性因子endostatin的血清值。结果与对照组相比,肺抑瘤膏组(P<0.05)、吉非替尼组(P<0.001)、联合药物组(P<0.001)肿瘤重量显著减少、肿瘤抑制率显著增加。与联合药物组相比,肺抑瘤膏组瘤重增加(P<0.001),吉非替尼组瘤重无显著差异。与对照组相比,肺抑瘤膏组(P<0.01)、吉非替尼组(P<0.001)、联合药物组(P<0.001)血清VEGF值均降低。与联合药物组相比,肺抑瘤膏组(P<0.001)和吉非替尼组(P<0.05)血清VEGF值均升高。与对照组相比,肺抑瘤膏组(P<0.05)、吉非替尼组(P<0.001)、联合药物组(P<0.001)血清endostatin值均升高。与联合药物组相比,肺抑瘤膏组(P<0.001)和吉非替尼组(P<0.05)血清endostatin值均降低。结论肺抑瘤膏联合吉非替尼在Lewis荷瘤小鼠体内具有抗肿瘤作用,其对肿瘤血管生成相关因子的调节作用强于单用吉非替尼。 Objective To elucidate the underlying mechanisms of Fei Yi Liu Gao( FYLG) combined with gefitinib against NSCLC. Methods The antiangiogenesis effect of FYLG combined with gefitinib on xenografted Lewis Lung Carcinoma( LLC,a mice model of NSCLC) in mice was investigated. Serum level of proangiogenic factors VEGF and antiangiogenic factor endostatin were assessed by ELISA. Results Compared with the control group,tumor weight was reduced and tumor inhibition( TI) was elevated in FYLG group( P 〈 0. 05),gefitinib group( P 0. 001),and FYLG combined with gefitinib group( P 〈 0. 001). Compared with the control group,the level of serum VEGF was significantly decreased in FYLG,gefitinib,FYLG combined with gefitinib groups( P 〈 0. 01). And the serum levels of endostatin were significantly increased in FYLG,gefitinib,FYLG combined with gefitinib groups( P 〈 0. 05). Conclusion Our study illuminated the antiangiogenesis effect of FYLG combined with gefitinib against LLC in mice.
作者 赵改霞 郑心
出处 《临床和实验医学杂志》 2018年第4期337-340,共4页 Journal of Clinical and Experimental Medicine
基金 山东省2013-2014年度中医药科技发展计划普通项目(编号:2013-095)
关键词 小鼠 Lewis荷瘤 肺抑瘤膏 吉非替尼 抗肿瘤血管生成 VEGF ENDOSTATIN Mice Lewis Lung Carcinoma FYLG Gefitinib Tumor angiogenesis inhibition VEGF Endostatin
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