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目的分析幽门螺杆菌感染胃上皮细胞过程中整合素β1亚基表达的变化,观察整合素β1对幽门螺杆菌感染胃上皮细胞GES-1凋亡及增殖的影响。方法将幽门螺杆菌与胃上皮细胞GES-1共培养,采用流式细胞术检测整合素β1的表达量变化;应用iRNA技术降低胃上皮细胞GES-1中β1亚基的表达;幽门螺杆菌感染胃上皮细胞及iRNA降低β1的表达后,采用流式细胞术检测细胞的凋亡,采用CCK-8法检测细胞增殖情况。结果幽门螺杆菌感染胃上皮细胞12、24、48h后空白对照组凋亡率分别为(10.80±0.71)%、(12.23±0.06)%和(12.30±2.12)%,Hp感染组凋亡率分别为(24.20±0.14)%、(30.05±2.47)%和(26.40±1.91)%,差异均有统计学意义(t值分别为-26.28、-7.701和-12.855,P<0.05);与幽门螺杆菌共培养6、24、48h胃上皮细胞增殖受到抑制,抑制率分别为(35.00±3.22)%、(40.96±2.45)%和(8.00±3.33)%;幽门螺杆菌与胃上皮细胞GES-1共培养24、48h流式细胞术检测整合素β1表达,空白对照组平均荧光强度(MFI)分别为(1616.33±24.70)和(1834.67±17.01),Hp感染组为(1484.00±60.89)和(1376.00±14.11),差异有统计学意义(t值分别为3.488和35.95,P<0.05);应用iRNA技术降低胃上皮细胞GES-1整合素β1亚基表达24、48h,对照组凋亡率分别为(18.75±3.59)%和(39.75±3.68)%,iRNA组凋亡率分别为(26.25±4.11)%和(55.30±5.57)%,差异有统计学意义(t值为-2.746和-4.656,P<0.05);胃上皮细胞中β1亚基的表达降低后细胞增殖受到抑制,24、36、48、72h抑制率分别为(6.16±1.07)%、(17.15±2.76)%、(10.84±1.34)%和(21.87±1.72)%。结论幽门螺杆菌能降低胃上皮细胞GES-1整合素β1亚基的表达,而且可能通过降低整合素β1亚基的表达促进上皮细胞GES-1的凋亡并抑制其增殖。
Objective To analyze the changes of integrin β1 subunit expression during the infection of gastric epithelial cells with Helicobacter pylori and to observe the effect of integrin β1 on the apoptosis and proliferation of gastric epithelial cells infected with Helicobacter pylori. Methods Helicobacter pylori and gastric epithelial cells were co-cultured with GES-1, and the expression of integrin β1 was detected by flow cytometry. The expression of β1 subunit of GES-1 in gastric epithelial cells was reduced by iRNA technique. Helicobacter pylori infection After gastric epithelial cells and iRNA decreased the expression of β1, the apoptosis of cells was detected by flow cytometry. The cell proliferation was detected by CCK-8 assay. Results The apoptotic rates of gastric epithelial cells infected with Helicobacter pylori at 12, 24 and 48 h were (10.80 ± 0.71)%, (12.23 ± 0.06)% and (12.30 ± 2.12)%, respectively. The difference was statistically significant (t = -26.28, -7.701 and -12.855, respectively, P <0.05), and were significantly higher than those of pyloric screw (24.0 ± 0.14)%, (30.05 ± 2.47)% and (26.40 ± 1.91) The inhibitory rates were (35.00 ± 3.22)%, (40.96 ± 2.45)% and (8.00 ± 3.33)%, respectively. The Helicobacter pylori and gastric epithelial cells GES-1 The mean fluorescence intensity (MFI) of the blank control group was (1616.33 ± 24.70) and (1834.67 ± 17.01), respectively, and the Hp infection group was (1484.00 ± 60.89) and (1376.00 ± 14.11), the difference was statistically significant (t = 3.488 and 35.95 respectively, P <0.05); iRNA technology was used to reduce the expression of integrin β1 subunit of GES-1 in gastric epithelial cells for 24,48 h, the apoptotic rates of control group were (18.75 ± 3.59)% and (39.75 ± 3.68)%, respectively. The apoptosis rates of iRNA group were (26.25 ± 4.11)% and (55.30 ± 5.57)%, respectively. The difference was statistically significant (t = -2.746 and -4.656, P <0.05); β1 subunit in gastric epithelial cells After 24 h, 36 h, 48 h and 72 h, the cell proliferation was inhibited (6.16 ± 1.07)%, (17.15 ± 2.76)%, (10.84 ± 1.34)% and (21.87 ± 1.72)%, respectively. Conclusion Helicobacter pylori can reduce the expression of GES-1 integrin β1 subunit in gastric epithelial cells, and may promote the apoptosis of GES-1 epithelial cells and decrease the proliferation of GES-1 cells by decreasing the expression of integrin β1 subunit.