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目的:探讨二氢杨梅素(DMY)对食管鳞癌细胞KYSE150和KYSE410增殖、凋亡及上皮间质转化(EMT)的影响。方法:采用不同浓度(0、25、50、100、150、200 μmol/L)的DMY处理KYSE150和KYSE410细胞24 h，采用细胞计数试剂盒8(CCK-8)法检测KYSE150和KYSE410细胞的半数抑制浓度(ICn 50)值。以0.5‰二甲基亚砜(DMSO)组为对照组、DMY、DMY+转化生长因子β1(DMY+TGF-β1)、转化生长因子β1(TGF-β1)为实验组，采用克隆形成实验和流式细胞术检测细胞增殖和凋亡情况，Transwell侵袭实验和划痕实验检测细胞侵袭和迁移能力，Western blot法检测半胱氨酸蛋白酶3(Caspase-3)、半胱氨酸天冬氨酸蛋白酶9(Caspase-9)、B淋巴细胞瘤2(Bcl-2)、Bcl-2相关x蛋白(Bax)、细胞信号转导分子Smad2/3(Smad2/3)、磷酸化细胞信号转导分子Smad2/3(p-Smad2/3)、波形蛋白(Vimentin)的蛋白表达水平。n 结果:DMY对KYSE410和KYSE150细胞ICn 50值分别为100.51和101.27 μmol/L。DMY组KYSE150和KYSE410细胞克隆形成数分别为(0.53±0.03)个和(0.31±0.03)个，均低于DMSO组[分别为(1.00±0.10)个和(1.00±0.05)个，均n P<0.05]，DMY组KYSE150和KYSE410细胞凋亡率分别为(1.84±0.22)%和(2.80±0.07)%，均高于DMSO组[分别为(1.00±0.18)%和(1.00±0.07)%，均n P<0.05]，DMY组KYSE150和KYSE410细胞侵袭数分别为(0.42±0.03)个和(0.29±0.05)个，均低于DMSO组[分别为(1.00±0.08)个和(1.00±0.05)个，均n P<0.05]，DMY组KYSE150和KYSE410细胞迁移率分别为(0.65±0.14)%和(0.40±0.17)%，均低于DMSO组[分别为(1.00±0.10)%和(1.00±0.08)%，均n P<0.05]。TGF-β1组KYSE150和KYSE410细胞克隆形成数分别为(1.01±0.08)个和(0.99±0.25)个，均高于DMY+TGF-β1组[分别为(0.73±0.10)个和(0.58±0.05)个，均n P<0.05]，TGF-β1组KYSE150和KYSE410细胞凋亡率分别为(0.81±0.14)%和(1.18±0.10)%，均低于DMY+TGF-β1组[分别为(1.38±0.22)%和(1.85±0.04)%，均n P<0.05]，TGF-β1组KYSE150和KYSE410细胞侵袭数分别为(1.19±0.11)个和(1.39±0.11)个，均高于DMY+TGF-β1组[分别为(0.93±0.09)个和(0.93±0.05)个，均n P<0.05]，TGF-β1组KYSE150和KYSE410细胞迁移率分别为(1.87±0.19)%和(1.32±0.04)%，均高于DMY+TGF-β1组[分别为(0.86±0.16)%和(0.77±0.12)%，均n P<0.05]。DMY组KYSE150和KYSE410细胞中Bax、Caspase-3、Caspase-9蛋白表达水平高于DMSO组，Bcl-2蛋白表达水平低于DMSO组(均n P<0.05)；DMY组KYSE150和KYSE410细胞中p-Samd2/3、Smad2/3和Vimentin蛋白的表达水平低于DMSO组(均n P<0.05)。TGF-β1组KYSE150和KYSE410细胞中Bax、Caspase-3、Caspase-9蛋白表达水平低于DMY+TGF-β1组，Bcl-2蛋白表达水平高于DMY+TGF-β1组(均n P<0.05)，DMY+TGF-β1组KYSE150和KYSE410细胞中Bax、Caspase-3、Caspase-9蛋白表达水平低于DMY组，Bcl-2蛋白表达水平高于DMY组(均n P<0.05)，TGF-β1组KYSE150和KYSE410细胞中p-Samd2/3、Smad2/3和Vimentin蛋白的表达水平高于DMY+TGF-β1组(均n P<0.05)。n 结论:DMY可以抑制TGF-β1介导的食管鳞癌细胞增殖及EMT且促进细胞凋亡。“,”Objective:To study the effects of dihydromyricetin (DMY) on the proliferation, apoptosis and epithelial mesenchymal transition (EMT) of esophageal squamous cell carcinoma (ESCC) cell KYSE150 and KYSE410.Methods:KYSE150 and KYSE410 cells were treated with different concentrations of DMY (0, 25, 50, 100, 150, 200 μmol/L) for 24 hours. The median inhibition concentration (IC n 50) values of KYSE150 and KYSE410 were detected by cell counting kit-8 (CCK-8) method. Then 0.5‰ dimethyl sulfoxide (DMSO) was used as control group, dihydromyricetin (DMY), dihydromyricetin and transforming growth factor-β1 (DMY+ TGF-β1), transforming growth factor-β1 (TGF-β1) were used as experimental group. Cell proliferation and apoptosis rates were measured by clonal formation and flow cytometry. Transwell invasion and wound healing assay were used to detect cell invasion and migration. The protein expression levels of Caspase-3, Caspase-9, Bcl-2, Bax, Smad2/3, phosphorylation-Smad2/3 (p-Smad2/3) and Vimentin were detected by western blot.n Results:The ICn 50 values of DMY on KYSE410 and KYSE150 cells were 100.51 and 101.27 μmol/L. The clone formation numbers of KYSE150 and KYSE410 in DMY group [(0.53±0.03) and (0.31±0.03)] were lower than those in DMSO group [(1.00±0.10) and (1.00±0.05), n P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in DMY group [(1.84±0.22)% and (2.80±0.07)%] were higher than those in DMSO group [(1.00±0.18)% and (1.00±0.07)%,n P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in DMY group [(0.42±0.03) and (0.29±0.05)] were lower than those in DMSO group [(1.00±0.08) and (1.00±0.05),n P<0.05]. The migration rates of KYSE150 and KYSE410 cells in DMY group [(0.65±0.14)% and (0.40±0.17)%] were lower than those in DMSO group [(1.00±0.10)% and (1.00±0.08)%,n P<0.05]. The clone formation numbers of KYSE150 and KYSE410 in TGF-β1 group [(1.01±0.08) and (0.99±0.25)] were higher than those in DMY+ TGF-β1 group [(0.73±0.10) and (0.58±0.05),n P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in TGF-β1 group [(0.81±0.14)% and (1.18±0.10)%] were lower than those in DMY+ TGF-β1 group [(1.38±0.22)% and (1.85±0.04)%,n P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in TGF-β1 group [(1.19±0.11) and (1.39±0.11)] were higher than those in DMY+ TGF-β1 group [(0.93±0.09) and (0.93±0.05),n P<0.05]. The migration rates of KYSE150 and KYSE410 cells in TGF-β1 group [(1.87±0.19)% and (1.32±0.04)%] were higher than those in DMY+ TGF-β1 group [(0.86±0.16)% and (0.77±0.12)%,n P<0.05]. The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY group were higher than those in DMSO group, while the protein expression level of Bcl-2 was lower than that in DMSO group (n P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in DMY group were lower than those in DMSO group (n P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in TGF-β1 group were lower than those in DMY+ TGF-β1 group, and the protein expression level of Bcl-2 was higher than that in DMY+ TGF-β1 group (n P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY+ TGF-β1 group were lower than those in DMY group, and the protein expression level of Bcl-2 was higher than that in DMY group (n P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in TGF-β1 group were higher than those in DMY+ TGF-β1 group (n P<0.05).n Conclusion:DMY can inhibit the proliferation and EMT of ESCC mediated by TGF-β1 and promote cell apoptosis.