目的 探究七方胃痛颗粒对转化生长因子-β1（TGF-β1）诱导人胃腺癌细胞AGS上皮间质转化（Epithelial-mesenchymal transition， EMT）过程的影响及其潜在分子机制。方法 为了探究七方胃痛颗粒对TGF-β1处理的AGS细胞增殖、迁移和侵袭的影响，实验分为四组：AGS细胞对照组，EMT空白模型组，中药血清组，TGF-β/smad通路抑制剂组，分别利用CCK8、细胞划痕实验和Transwell实验检测细胞增殖、迁移和侵袭能力。此外，通过免疫荧光检测EMT过程中相关蛋白（E-cadherin、N-cadherin、14-3-3ζ、Smad2和p-Smad2/3）的表达水平。结果 与AGS细胞对照组相比，TGF-β1诱导EMT过程，显著促进AGS细胞增殖、迁移和侵袭，下调了E-cadherin的表达，上调了N-cadherin、14-3-3ζ、Smad2和p-Smad2/3的表达；与EMT空白模型组相比，中药血清组、TGF-β/smad通路抑制剂组显著抑制了细胞增殖、迁移和侵袭，上调了E-cadherin的表达，降低了N-cadherin、14-3-3ζ、Smad2和p-Smad2/3的表达。结论 七方胃痛颗粒通过调控TGF-β/smad信号通路从而抑制人胃腺癌AGS细胞的EMT过程。

Objective To investigate the effect of Qifangweitong granule on the process of transforming growth factor-β1 (TGF-β1)-induced human gastric adenocarcinoma cell AGS epithelial-mesenchymal transition (EMT) and its potential molecular mechanism.Methods In order to explore the effect of Qifangweitong granule on the proliferation, migration and invasion of TGF-β1 treated AGS cells, the experiment was divided into four groups: AGS cell control group, EMT blank model group, Chinese medicine serum group, TGF-β/smad pathway inhibitor group. CCK8, cell scratch test and Transwell test were used to detect cell proliferation, migration and invasion ability, respectively. In addition, the expression levels of related proteins (E-cadherin, N-cadherin, 14-3-3ζ, Smad2 and p-Smad2/3) were detected by immunofluorescence.Results Compared with the AGS cell control group, TGF-β1 induced EMT process, significantly promoted AGS cell proliferation, migration and invasion, down-regulated the expression of E-cadherin, and up-regulated N-cadherin, 14-3-3ζ, Smad2 and p-Smad2/3 expression. Compared with the EMT blank model group, the Chinese medicine serum group and the TGF-β/smad pathway inhibitor group significantly inhibited cell proliferation, migration and invasion, up-regulated the expression of E-cadherin, and reduced N-cadherin, 14-3-3ζ, Smad2 and p-Smad2/3 expression.Conclusion Qifangweitong granule inhibits the EMT process of human gastric adenocarcinoma AGS cells by regulating the TGF-β/smad signaling pathway.