参芪金康胶囊抗肿瘤作用的实验研究  

Experimental Study on Antitumor Effects of Shen Qi Jin Kang (SQJK)

作　　者：刘朝阳[1] 王德昌[1] 付招娣[2] 刘红岩[2] 梁智[1] 程冬婉[1] 梁军林[1] 梁建明[1] 

机构地区：[1]中国医学科学院中国协和医科大学肿瘤研究所肿瘤医院,北京100021 [2]中国医学科学院中国协和医科大学药物研究所,北京100050

出　　处：《癌症》2006年第8期983-989,共7页Chinese Journal of Cancer

摘　　要：背景与目的:参芪金康胶囊是由黄芪、人参、姜黄等13味中药提取的有效成分组成的复方制剂,是院内制剂,在临床应用可改善患者全身情况,提高其生活质量。本研究目的是观察参芪金康胶囊对小鼠移植性肿瘤和人肿瘤细胞裸鼠移植瘤的体内抗肿瘤作用,以及体外对人肿瘤细胞株的抑瘤活性,并探讨其作用机理。方法:MTT法检测参芪金康胶囊体外对人肿瘤细胞的增殖抑制作用;观察其对小鼠和裸鼠体内移植肿瘤的抑制作用;应用流式细胞仪分析和电镜方法观察参芪金康胶囊诱导MCF-7和MA891细胞凋亡作用;使用端粒酶活性检测试剂盒检测参芪金康胶囊对人肺癌细胞A549端粒酶活性的影响。结果:参芪金康胶囊体外对A549、U251、MCF-7、Ketr-3、EJ和A2780等细胞具有明显的抑制作用,IC50值分别为30.954、31.746、37.220、40.366、41.398和45.083μg/ml。1.8g/kg、3.6g/kg生药对小鼠肿瘤MA891抑瘤率分别为50.84%和56.49%,对H22抑瘤率分别为48.91%和59.62%,对S180抑瘤率分别为40.88%和55.70%;对人前列腺癌细胞PC-3(M)裸鼠移植瘤抑瘤率分别为62.50%和70.76%,对MCF-7抑瘤率分别为47.83%和58.66%,对Ketr-3抑瘤率分别为30.06%和50.18%,与对照组比较差异均有显著性。流式细胞仪分析,在参芪金康胶囊作用后MA891和MCF-7都出现凋亡峰;电镜观察,MA891和MCF-7细胞发生凋亡,表现为细胞固缩、核染色质边移,呈马蹄形或半月形。参芪金康胶囊体外(15～60μg/ml)作用48h,A549细胞端粒酶活性明显降低。结论:参芪金康胶囊在体内、外对动物和人肿瘤细胞均有明显抑制作用,其作用机理可能与诱导细胞凋亡和降低端粒酶活性有关。BACKGROUND ＆ OBJECTIVE： SHEN QI JIN KANG （SQJK） capsule is a complex preparation, consisting of effective components extractied from radix astragali, ginseng, curcuma, etc. It has been demonstrated to be able to decrease tumor volume, increase life quality and prolong survival time in clinic application. The study was to investigate the antitumor effects of SQJK capsule in vivo and in vitro, and further explore the possible mechanisms. METHODS： The proliferation of cancer cells treated with SQJK was measured by MTT assay in twelve cell lines; cell apoptosis was observed under an electric microscopic and detected by flow cytometry in MCF-7 and MA891 cells; altered telomerase activity in A549 cells was examined by a telomerase activity detection kit. Furthermore, the inhibitory effect of SQJK on tumors was also surveyed in vivo by using mice and nude mice models bearing transplanted tumors RESULTS： Inhibitory concentration 50% （IC50） of SQJK on A549, U251, MCF-7, Ketr-3, EJ, and A2780 cells was 30.954 μg/ml, 31.746 μg/ml, 37.220μg/ml, 40.366μg/ml, 41.398 μg/ ml, and 45.083μg/ml, respectively. Typical sub-G1 peaks, indicating the occurrence of apoptosis, were revealed in MA891and MCF-7 cells treated with SQJK. Morphological changes including cell shrinkage and condensation of chromosomes were observed. The telomerase activity of A549 was inhibited after 48 h of SQJK treatment. SQJK 1.8 g/kg inhibited the weights of transplanted tumors （MA891, H22, S180 in mice and PC-3 （M）, MCF-7 and Ketr-3 in nude mice ） by 50.84%, 48.91%, 40.88%, 62.50%, 47.83% and 30.06%, while SQJK 3.6 g/kg inhibited the weights by 56.49%, 59.62%, 55.70%, 70.76%, 58.66% and 50.18%, respectively. CONCLUSION： SQJK has demonstrated antitumor bioactivity both in vitro and in vivo, which may be related to its effects of inducing apoptosis and decreasing telomerase activity.

关 键 词：参芪金康胶囊/药理学 移植性肿瘤 人肺癌细胞A549 凋亡 端粒酶 小鼠 

分 类 号：R285[医药卫生—中药学]