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作 者:李晓花[1] 李海涛[1] 金玲钰 牛迎凤[1] 张丽霞[1]
机构地区:[1]西双版纳州傣药南药重点实验室中国医学科学院北京协和医学院药用植物研究所云南分所,云南景洪666100
出 处:《中国实验方剂学杂志》2017年第2期104-108,共5页Chinese Journal of Experimental Traditional Medical Formulae
基 金:中央级公益性科研院所基本科研业务专项(YZYN-15-01);景洪市科技三项费专项([2014]-43-2)
摘 要:目的:探讨傣百解乙酸乙酯提取物(ethyl acetate fraction,EFA)诱导人肺癌A549裸鼠移植瘤生长的抑制作用及作用机制。方法:建立人肺癌裸鼠移植瘤模型,随机分为模型组,EFA高、中、低剂量(200,100,50 mg·kg-1)组,环磷酰胺组和消癌平组,每组6只。给药3周后剥离瘤组织,比较各组肿瘤质量,计算抑制率;末端脱氧核苷酸转移酶介导的d UTP缺口末端标记测定法(TUNEL)检测各组移植瘤组织中的细胞凋亡情况;免疫组化法(immunhistochemical staining,IHC)检测瘤组织中p53,B淋巴细胞瘤-2(Bcl-2)和Bcl-2相关X蛋白(Bax)蛋白的表达。结果:与模型组比较,EFA高、中、低剂量组对肿瘤组织具有明显的抑制作用(P<0.05,P<0.01)。TUNEL法检测结果显示EFA给药处理后,与模型组比较,肿瘤细胞凋亡明显增多。免疫组化结果显示,与模型组比较,各给药组移植瘤p53和Bax蛋白表达明显升高,而Bcl-2表达降低。结论:EFA对人肺癌A549裸鼠移植瘤具有明显的抑制作用,其机制可能与上调p53和Bax蛋白的表达,降低Bcl-2蛋白的表达,诱导肺癌细胞凋亡相关。Objective: To study the inhibitory effect and mechanism of ethyl acetate fraction( EFA)extracted from Daibaijie on A549 human lung cancer cell line in nude mice. Method: Xenotransplanted tumor models of A549 tumor cells in nude mice were established,and were randomly divided into model group,EFA high-dose,middle-dose and low-dose( 200,100,50 mg·kg^- 1) groups,Xiaoaiping group and cyclophosphamide group. There were six mice in each group. Tumor weights were observed to calculate the inhibitory rate after three weeks of administration. The apoptosis rates were measured by terminal dexynucleotidyl transferase( Td T)-mediated d UTP nick end labeling( TUNEL) staining method and the protein expression levels of p53,B-cell lymphoma-2( Bcl-2) and Bcl-2 associated X protein( Bax) were detected by immunhistochemical staining( IHC).Result: As compared with the model group,EFA can significantly inhibit the growth of A549 xenografts in a dose manner( P〈0. 05,P〈0. 01). TUNEL assay results showed that the apoptosis rate of tumor cells increased significantly after treatment with EFA. The immunohistochemical results showed that,as compared with model group,the protein expression level of Bcl-2 was decreased,while the expression levels of p53 and Bax were increased in nude mice after treatment with EFA. Conclusion: EFA has a significant inhibitory effect on human lung cancer A549 in nude mice. The mechanism may be related to up-regulating the expression of p53 and Bax protein,decreasing the expression of Bcl-2 protein,and inducing apoptosis of lung cancer cells.
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