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走马胎中化合物AG4对人鼻咽癌细胞裸鼠移植瘤的影响

作者:晓兰 整理 来源:金宝搏网站登录技巧 日期:2015-06-10
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         为了建立研究走马胎中化合物AG4对人鼻咽癌细胞裸鼠移植瘤生长的影响,研究者发表《走马胎中化合物AG4对人鼻咽癌细胞裸鼠移植瘤的影响》研究,该文章发表于2015年1期的《中国药物应用与监测》上,研究表明AG4在裸鼠体内对人鼻咽癌细胞有较强的抑制作用,对裸鼠没有明显的毒副作用,其作用机制可能与激活线粒体途径诱导肿瘤细胞凋亡有关。

关键字:  走马胎 |  |  |  |  | 鼻咽癌 |  |  |  |  | Bcl-2家族 |  |  |  |  | 裸鼠 

        为了建立研究走马胎中化合物AG4对人鼻咽癌细胞裸鼠移植瘤生长的影响,研究者发表《走马胎中化合物AG4对人鼻咽癌细胞裸鼠移植瘤的影响》研究,该文章发表于2015年1期的《中国药物应用与监测》上,研究表明AG4在裸鼠体内对人鼻咽癌细胞有较强的抑制作用,对裸鼠没有明显的毒副作用,其作用机制可能与激活线粒体途径诱导肿瘤细胞凋亡有关。

        建立人鼻咽癌细胞裸鼠皮下移植瘤模型,以抑瘤率为指标研究化合物AG4的体内抑瘤作用及AG4干预对裸鼠的一般情况(体质量、活动、食欲等)的影响;同时采用实时荧光定量PCR法观察AG4对肿瘤内凋亡相关基因表达的影响。

        阳性药顺铂组(2.00 mg•kg-1)对荷瘤裸鼠的抑瘤率为49.41%,3.02 mg•kg-1AG4组的抑瘤率为42.34%,AG4对裸鼠体质量及肝、脾、肾的脏器指数没有明显影响;AG4能明显升高Bax和Bad基因的相对表达量,降低Bcl-2基因的相对表达量。

        英文摘要:

        Inhibition of compound AG4 fromArdisia gigantifolia Stapf. on xenograft tumor growth of human nasopharyngeal carcinoma in nude mice

        Abstract: Objective:To investigate the influence of compound AG4 derived fromArdisia gigantifolia Stapf. on xenograft tumor of human nasopharyngeal carcinoma (NPC) in nude mice.Methods: Human NPC nude mice model were established, and the inhibition rate (IR) was the index to evaluate the tumor growth suppression of AG4in vivo. Simultaneously, general conditions (weight, action, appetite) of nude mice and the expression of Bcl-2, Bad and Bax mRNA by real time PCR method were observed during AG4 interference.Results: The IR of positive control group (cisplatin 2.00 mg•kg-1) and AG4 group (3.02 mg•kg-1) was 49.41% and 42.34% respectively. The effect of AG4 on the weight lose of nude mice was not significant comparing with negative control group, and the toxicity of AG4 to the vital organs (liver, spleen and kidney) and immunity index (spleen index) was not obvious in short period. AG4 could increase the Bax and Bad mRNA expression, and decrease the Bcl-2 mRNA expression.Conclusion:AG4 had obvious inhibition effects on xenograft tumor in human NPC nude mice, and with no outstanding adverse effects, the mechanisms may relate to the induction of tumor apoptosis due to the activation of mitochondria signal pathway.

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