| 引用本文: |
谢金魁 曹建国 张安强 王娟.蛞蝓提取物抗肺癌的作用机制研究[J].湖南中医药大学学报,2011,31(7):6-10[点击复制] |
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| 蛞蝓提取物抗肺癌的作用机制研究 |
| 谢金魁曹建国张安强王娟 |
| (广州汉方现代中药研究开发有限公司广东广州520240;湖南师范大学医学院药物工程实验室湖南长沙410006
浙江工业大学生物环境工程学院，浙江杭州310014.南华大学药物药理研究所，湖南衡阳421001)) |
| 摘要: |
| 目的 探讨蛞蝓提取物((EL-3)抗肺癌的作用机制〔方法(1)}}化尿uw n,}核} (BrdU)掺入法观察EL-3对
人源性肺癌As49细胞的掺入抑制率;(2 > n,f n,}橙/嗅化乙n} (AO/EB)染色荧光显微镜，观察EL-3诱发As49凋亡细
胞的形态，计数凋亡细胞;PI染色流式细胞术((FC M)分析细胞周期和凋亡率〔(3)DNA琼脂糖凝胶电泳法，观察凋亡
细胞“梯形”DNA条带;(4)免疫组化DAB染色法观察EL-3对PCNA,VEGF,CD31的蛋白表达的影响、结果(1)单
用} }'au提取物100 N.,g/mL浓度的EL-3对人肺癌细胞As49核酸合成抑制率((IR)高达63.s90Ic;与空白对照组(0)和
溶媒对照组((7.s4%)比较差异有统计学意义(P<0.01)，且呈剂量依赖性，其半数抑制浓度为28.s3 N.,g/mL; (2)与化疗
药合用有增效作用:EL-3与顺铂合用能显著提高顺铂对As49细胞的核酸合成抑制率:EL-3低、中、高剂量组，使
单用DDP的IR由14.01%分别提高到44.s0Ic ,48.96%和67.os%(P
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| 关键词: 蛞蝓 蛤蝙提取物 肺癌细胞 凋亡 裸鼠 |
| DOI： |
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| 基金项目:广州市重大攻关引导项日((200325-E31010) |
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| Research of EL-3 on anti-lung cancer mechanism |
| XIE Jin-kui, CAO Jian-guo, ZHANG An-qiang, WANG Juan |
| ((Guangzhou Hanfang Pharmaceuticai Company Limited, Guangzhou, Guangdong, 520240
China) |
| Abstract: |
| To investigate the mechanism of extract of limax (EL-3) on anti-
lung cancer. Methods (1) BrdU infiltration method was used[()observe the inhibiting rates of
EL-3 on the human lung cancer A549 cells. (2) The morphology of A549 cells apoptosis in-
duced by EL-3 was determined and counted with the acridine orange/ethidium bromide (AO/EB)
staining, and the cell cycle and apoptosis were analyzed with FCM. (3) The ladder-like DNA
bands of apoptosis cells was observed by the DNA garose gelatin electrophoresis. (4) The protein
expression levels of PCNA, VEGF and CD3 affected by EL-3 were detected with Immunochisto-
chemical technique and DAB staining. Results (1) EL-3 using only in concentration 100 N.,g/mL
[()induce A549 cells, the inhibiting rate was 63.59%.，which was significant compared with
black group (0) and solvent group (7.54%) (P<0.01). (2) EL-3 was me)二effective combined
with chemotherapeutics and enhanced the effect of CDDP on nucleic acid synthesis inhibition
rate of A549. EL-3 in low, middle and high dose groups, the IR of DDP used only were in-
creased to14.01% 44, 5%, 48.96% and 67.05%(P<0.01); when IC50 in 20.62 N.,g/mL, EL-3 used
with paclitaxel significantly improved the inhibition of A549 cell nucleic acidsynthesis. EL-3 in
low, middle and high dose groups enhanced the IR of TAX used only on A549 cell were re-
spectively increased from 21.79%[()58.35%，66.13% and 73.67% (P<0.05), and the IC50 was |
| Key words: slug: EL-3二lung-cancer:
angioge nesis:
nude
mouse |
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