目的:探讨丙泊酚对人胃癌细胞增殖、迁移和侵袭的影响及其分子机制。方法:采用四甲基偶氮唑蓝(MTT)法检测不同浓度丙泊酚对人胃癌MGC-803和HGC-27细胞活力的影响。将MGC-803细胞分为对照组和丙泊酚组，Hoechst 33258染色和电镜检测两组细胞凋亡率，Transwell实验检测两组细胞迁移率和侵袭率。随后将细胞分为对照组、丙泊酚组和丙泊酚＋miR-195i组，实时荧光定量PCR(qRT-PCR)检测细胞中miR-195相对表达量，蛋白质印迹法检测细胞中Janus激酶/信号转导与转录激活子(JAK/STAT)信号通路蛋白的表达。结果:0、1、5、10、20 mg/L丙泊酚作用24 h，MGC-803细胞活力分别为(100.00±4.96)%、(94.63±3.15)%、(77.38±6.73)%、(63.82±8.42)%和(35.94±7.01)%，组间差异具有统计学意义(n F＝5.148，n P<0.001)，与0 mg/L丙泊酚相比，5、10和20 mg/L丙泊酚作用下细胞活力显著降低(均n P<0.05)。同时丙泊酚作用48和72 h也可显著降低MGC-803细胞活力。HGC-27细胞中也检测到类似的结果。Hoechst 33258染色结果显示，对照组阳性细胞百分率为(3.73±1.81)%，丙泊酚组为(25.44±1.05)%，两组间差异具有统计学意义(n t＝6.415，n P<0.001)。电镜结果显示，对照组细胞凋亡率为(4.60±1.36)%，丙泊酚组为(28.15±1.99)%，两组间差异具有统计学意义(n t＝10.729，n P<0.001)。Transwell结果显示，对照组细胞迁移率为(53.94±4.62)%，丙泊酚组为(21.28±3.98)%；对照组细胞侵袭率为(62.38±6.75)%，丙泊酚组为(33.81±4.92)%，两组间差异均具有统计学意义(n t＝4.628，n P<0.001；n t＝6.418，n P<0.001)。qRT-PCR结果显示，对照组、丙泊酚组、丙泊酚＋miR-195i组miR-195相对表达量分别为0.58±0.09、1.24±0.22、0.63±0.16，3组间差异具有统计学意义(n F＝1.547，n P＝0.001)；与对照组相比，丙泊酚组细胞miR-195表达显著增加(n P<0.001)。与丙泊酚组相比，丙泊酚＋miR-195i组细胞miR-195表达显著降低(n P<0.001)。蛋白质印迹检测结果显示，对照组、丙泊酚组、丙泊酚＋miR-195i组磷酸化Janus激酶1(p-JAK1)蛋白相对表达量分别为1.18±0.36、0.27±0.08、0.58±0.11，3组磷酸化信号转导与转录激活因子3(p-STAT3)蛋白相对表达量分别为0.83±0.16、0.21±0.07、0.72±0.13，差异均有统计学意义(n F＝1.655，n P<0.001；n F＝2.520，n P<0.001)；与对照组相比，丙泊酚组细胞p-JAK1和p-STAT3蛋白相对表达量显著降低(n P<0.001；n P＝0.001)；与丙泊酚组相比，丙泊酚＋miR-195i组细胞p-JAK1和p-STAT3蛋白相对表达量显著增加(n P＝0.003；n P＝0.004)。n 结论:丙泊酚可抑制胃癌细胞MGC-803的细胞增殖、迁移和侵袭，促进其凋亡，其机制可能与丙泊酚促进miR-195表达并抑制JAK/STAT信号通路活性有关。“,”Objective:To investigate the effect of propofol on the proliferation, migration and invasion of human gastric cancer cells and its molecular mechanism.Methods:The cell viabilities of human gastric MGC-803 and HGC-27 cells under different concentration of propofol were detected by methyl thiazolyl tetrazolium (MTT) method. MGC-803 cells were divided into control group and propofol group. Hoechst 33258 staining and electron microscopy were used to detect the apoptosis rates of the two groups of cells. Transwell experiment was used to detect the migration and invasion rates of the two groups of cells. The cells were then divided into control group, propofol group and propofol + miR-195i group. Real-time fluorescent quantitative PCR (qRT-PCR) was used to detect the relative expression of miR-195 in the cells. Western blotting was used to detect the expressions of Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway proteins.Results:At 24 h, the cell viabilities of MGC-803 cells under the action of 0, 1, 5, 10 and 20 mg/L propofol respectively were (100.00±4.96)%, (94.63±3.15)%, (77.38±6.73)%, (63.82±8.42)% and (35.94±7.01)%, with a statistically significant difference (n F=5.148, n P<0.001). The cell viabilities of MGC-803 cells under the action of 5, 10 and 20 mg/L propofol were decreased significantly compared to that under the action of 0 mg/L propofol (alln P<0.05). At the same time, the effects of propofol for 48 and 72 h could also significantly reduce the viabilities of MGC-803 cells. Similar results were also detected in HGC-27 cells. The results of Hoechst 33258 staining showed that the percentage of positive cells in the control group was (3.73±1.81)%, and that in the propofol group was (25.44±1.05)%, with a statistically significant difference (n t=6.415, n P<0.001). The results of electron microscopy showed that the apoptosis rate in the control group was (4.60±1.36)%, and that in the propofol group was (28.15±1.99)%, with a statistically significant difference (n t=10.729, n P<0.001). Transwell results showed that the cell migration rate in the control group was (53.94±4.62)%, and that in the propofol group was (21.28±3.98)%; the cell invasion rate in the control group was (62.38±6.75)%, and that in the propofol group was (33.81±4.92)%, and there were statistically significant differences (n t=4.628, n P<0.001;n t=6.418, n P<0.001). qRT-PCR results showed that the relative expressions of miR-195 in the control group, propofol group and propofol + miR-195i group were 0.58±0.09, 1.24±0.22 and 0.63±0.16, with a statistically significant difference (n F=1.547, n P=0.001). miR-195 expression was increased significantly in the propofol group compared to the control group (n P<0.001). Compared with the propofol group, miR-195 expression in the propofol + miR-195i group was decreased significantly (n P<0.001). Western blotting results showed that the relative expressions of phosphorylase Janus kinase 1 (p-JAK1) protein in the control group, propofol group and propofol + miR-195i group were 1.18±0.36, 0.27±0.08 and 0.58±0.11; the relative expressions of phosphorylase signal transducer and activator of transcription 3 (p-STAT3) protein in the three groups were 0.83±0.16, 0.21±0.07 and 0.72±0.13, and there were statistically significant differences (n F=1.655, n P<0.001;n F=2.520, n P<0.001). The expressions of p-JAK1 and p-STAT3 protein in the propofol group were decreased significantly compared to the control group (n P<0.001;n P=0.001). The expressions of p-JAK1 and p-STAT3 protein in the propofol + miR-195i group were increased significantly compared to the propofol group (n P=0.003; n P=0.004).n Conclusion:Propofol can inhibit the cell proliferation, migration and invasion of gastric cancer MGC-803 cells, and promote its apoptosis. Its mechanism may be related to the promotion of miR-195 expression and inhibition of JAK/STAT signal pathway activity.