Objective To investigate the inhibitory effects of allicin on TGF-β1 -induced epithelium mesenchymal transition (EMT)of pancreatic cancer cells and its mechanism.Methods The pancreatic cancer cell line PANC-1 in loga-rithmic growth phase were routinely cultured and then were randomly divided into allicin +TGF-β1 group,allicin group, TGF-β1 group and the control group.The PANC-1 cells in the former three groups were respectively treated with 10 ng/mL TGF-β1 +5 μg/mL allicin,5 μg/mL allicin,and 10 ng/mL TGF-β1 ,and the control group without any treatment.MTT assay was used to detect cell proliferation;scratch test,Transwell chamber experiment were used to measure the migration and invasion of pancreatic cancer cell,and RT-PCR was applied to detect the E-Cadherin,Viminten and NF-κB expres-sion.Results MTT showed that after allicin intervention,the cell proliferation of pancreatic cancer was inhibited,IC50 at 24 and 48 h was 69.44,and 100.9 μmol/L,which was in a time-and dose-dependent manner.The scratch test showed the migration rates at 8 h of the control group,allicin +TGF-β1 group,allicin group and TGF-β1 group were 0.56 ±0.11, 0.10 ±0.07,0.09 ±0.05,and 0.61 ±0.23;at 24 h ,they were 1.00 ±0.00,0.74 ±0.20,0.40 ±0.05,and 1.00 ± 0.00.Transwell chamber experiment showed the invasion rates of the control group,allicin +TGF-β1 group,allicin group and TGF-β1 group were 2.15 ±0.04,1.98 ±0.14,1.01 ±0.01 and 2.93 ±0.02,and statistically significant difference was found between allicin group and the other three groups (all P <0.05).The RT-PCR showed that compared with the control group,E-cadherin expression was significantly decreased,and Vimentin expression was significantly increased in the TGF-β1 group (all P <0.05).Compared with TGF-β1 group,the E-candherin was up-regulated,Vimentin was down-regulated and the NF-κB expression was also down-regulated in the allicin + TGF-β1 group and allicin group (all P <0.05).Conclusion Allicin has a blocking effect on TGF-β1 -induced EMT of pancreatic cancer,which can inhibit the EMT of pancreatic cancer cells by regulating NF-κB signaling pathway.%目的：探讨大蒜素对 TGF-β1诱导的胰腺癌细胞上皮－间充质转化（EMT）的抑制作用及机制。方法常规培养胰腺癌细胞株 PANC-1细胞，取对数生长期细胞，随机分为大蒜素＋TGF-β1组、大蒜素组、TGF-β1组及空白对照组，前三组分别以 TGF-β110 ng／mL ＋大蒜素5μg／mL、大蒜素5μg／mL、TGF-β110 ng／mL 处理 PANC-1细胞，空白对照组不予干预。应用 MTT 法检测细胞增殖情况；划痕试验、Transwell 小室试验测定胰腺癌细胞的迁移、侵袭能力。RT-PCR 法检测各组 E-Cadherin、Viminten 及 NF-κB 表达。结果 MTT 结果显示大蒜素干预后胰腺癌细胞增殖受到抑制，24 h 与48 h 的 IC50分别为69．44、100．90μmol／L，呈时间和剂量依赖性；划痕试验显示空白对照组、大蒜素＋TGF-β1组、大蒜素组及 TGF-β1组8 h 迁移率分别为0．56±0．11、0．10±0．07、0．09±0．05、0．61±0．23；24 h 迁移率分别为1．00±0．00、0．74±0．20、0．40±0．05、1．00±0．00。Transwell 小室试验显示，空白对照组、大蒜素＋TGF-β1组、大蒜素组及 TGF-β1组的侵袭率分别为2．15±0．04、1．98±0．14、1．01±0．01、2．93±0．02，大蒜素组与其他三组比较差异有统计学意义（P 均＜0．05）；RT-PCR 结果显示，与空白对照组相比，TGF-β1组 E-cadherin 表达明显下调（P 均＜0．05），Vimentin 表达则明显上调（P 均＜0．05）。与 TGF-β1组相比，大蒜素＋TGF-β1组及大蒜素组 E-candherin 表达上调，Vimentin 表达下调；同时，NF-κB 的表达亦明显下调（P 均＜0．05）。结论大蒜素能阻断 TGF-β1诱导的胰腺癌EMT 效应，其可能通过抑制 NF-κB 信号通路抑制胰腺癌细胞发生 EMT。
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