| 张翠翠,李强.虎杖苷通过蛋白激酶 B信号通路影响胃癌细胞增殖凋亡[J].安徽医药,2021,25(9):1708-1712. |
| 虎杖苷通过蛋白激酶 B信号通路影响胃癌细胞增殖凋亡 |
| Polydatin affects the proliferation and apoptosis of gastric cancer cells through Akt signaling pathway |
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| DOI：10.3969/j.issn.1009-6469.2021.09.003 |
| 中文关键词: 虎杖 蛋白质丝氨酸苏氨酸激酶 胃癌 蛋白激酶 B信号 凋亡 周期 |
| 英文关键词: Fallopia japonica Protein-serine-threonine kinases Gastric cancer Akt signal Apoptosis Cycle |
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| 中文摘要: |
| 目的研究虎杖苷对胃癌细胞 SGC-7901增殖和凋亡的影响和机制。方法虎杖苷处理胃癌细胞 SGC-7901，MTT法检测增殖，平板克隆实验检测克隆形成能力，碘化丙啶( PI)单染法检测细胞周期分布，膜联蛋白 V-异硫氰酸荧光素 /碘化丙啶(Annexin V-FITC/PI)双染法检测细胞凋亡，蛋白质印迹法( Western blotting)检测细胞周期蛋白 D1(cyclin D1)、周期蛋白依赖性激酶 4(CDK4)、 Bcl-2相关 X(Bax)、剪切型胱天蛋白酶 -3(Cleaved-caspase-3)、磷酸化 -蛋白激酶 B(p-Akt)蛋白表达。用蛋白激酶 B(Akt)信号激活剂和虎杖苷联合处理胃癌细胞 SGC-7901，检测细胞增殖、克隆、周期、凋亡变化。结果虎杖苷处理以后的胃癌细胞 SGC-7901增殖能力下降［( 0.58±0.06)比( 0.20±0.01)］，细胞克隆形成数目减少［( 118.54±10.65)个比( 69.52±7.91)个］，细胞凋亡增多［( 2.97±0.32)%比( 17.45±1.69)%］，细胞 G0/G1比例升高［( 50.47±3.25)%比( 67.13±3.84)%］，cyclin D1、 CDK4蛋白表达减少， Bax、Cleaved-caspase-3蛋白表达水平升高， p-Akt蛋白水平降低［(0.51±0.05)比( 0.24±0.03)］。 Akt信号激活剂处理可以逆转虎杖苷对胃癌细胞 SGC-7901增殖、克隆抑制和周期阻滞、凋亡促进作用。结论虎杖苷通过抑制 Akt信号通路阻碍胃癌细胞增殖并诱导细胞凋亡。 |
| 英文摘要: |
| Objective To study the effect and mechanism of polydatin on proliferation and apoptosis of gastric cancer cell line SGC-7901.Methods Polydatin was used to treat gastric cancer cell SGC-7901, MTT was used to detect proliferation, and plate cloning experiment was used to detect clone formation ability, cell cycle distribution was detected by PI single staining, apoptosis was detected byAnnexin V-FITC/PI double staining, and cyclin D1, CDK4, Bax, Cleaved-caspase-3 and p-Akt protein were detected by Western blotting. Gastric cancer cell line SGC-7901 was treated with Akt signaling activator combined with polydatin, and cell proliferation, cloning, cycle and apoptosis were detected.Results After treatment with polydatin, the proliferation of gastric cancer cells SGC-7901 decreased [(0.58±0.06) vs. (0.20±0.01)], the number of cell clones decreased [(118.54±10.65) vs. (69.52±7.91)], the apoptosis increased [(2.97±0.32)% vs. (17.45±1.69)%], the ratio of G0/G1 increased [(50.47±3.25)% vs. (67.13±3.84)%], the expression of cyclin D1 and CDK4 decreased, and the expression of Bax and Cleaved-caspase-3 elevated, p-Akt protein level were reduced [(0.51±0.05) vs. (0.24±0.03)]. Akt signal activator treatment could reverse the proliferation, clonal inhibition, cell cycle arrest and apoptosis promotion of polydatin in gastric cancer cell line SGC-7901.Conclusion Polydatin inhibits proliferation of gastric cancer cells and induces apoptosis by inhibiting Akt signaling pathway. |
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