论文部分内容阅读
目的:研究不同浓度的温郁金二萜类化合物C对3种不同分化阶段的胃腺癌细胞株增殖和凋亡的影响,来揭示其对不同类型胃癌的作用和机制。方法:取0、10、20、40、80μg/m L浓度的温郁金二萜类化合物C体外作用于人正常胃黏膜上皮细胞(GES-1),人脐静脉细胞(HUVEC),低分化胃腺癌细胞株MKN45,中分化胃腺癌细胞株SGC-7901和高分化胃腺癌细胞株MKN 28 24、48、72、96h,用MTT法检测5种细胞株的生长曲线;采用流式细胞技术和Annexin V-FITC/PI双染法检测各细胞的凋亡率和细胞周期;采用Western blot技术检测各细胞株中凋亡相关蛋白Bcl-2和Bax的表达。结果:1与温郁金二萜类化合物C对各分化程度的胃腺癌细胞均有一定的抑制作用,呈现浓度依赖性,其中对SGC-7901的抑制最为明显;而对人GES-1和HUVEC的抑制作用相对不明显。2温郁金二萜类化合物C对3种胃腺癌细胞株的细胞周期均有抑制作用。3温郁金二萜类化合物C能有效地诱导各胃腺癌细胞株凋亡,其作用亦有一定的浓度依赖性;对SGC-7901作用最明显。4温郁金二萜类化合物C能不同程度的抑制各胃腺癌细胞株抗凋亡蛋白Bcl-2的表达,上调促凋亡蛋白Bax的表达;其作用具有浓度依赖性。结论:温郁金二萜类化合物C能在对GES-1和HUVEC安全的浓度范围内通过细胞毒性作用和阻制胃癌细胞分裂周期作用来抑制胃癌细胞的增殖;通过下调抗凋亡蛋白Bcl-2和上调促凋亡蛋白Bax的表达来诱导胃癌细胞的凋亡,从而发挥抗胃癌的作用。
OBJECTIVE: To study the effects of different concentration of diterpenoid C on the proliferation and apoptosis of gastric adenocarcinoma cell lines in three different differentiation stages to reveal its effect on different types of gastric cancer. Methods: Dhtosporin C from 0, 10, 20, 40 and 80 μg / mL was used to treat human normal gastric epithelial cells (GES-1), human umbilical vein cells (HUVECs), poorly differentiated gastric adenocarcinoma Cell line MKN45, moderately differentiated gastric adenocarcinoma cell line SGC-7901 and well-differentiated gastric adenocarcinoma cell line MKN 28 24, 48, 72, 96h. The growth curves of 5 cell lines were detected by MTT assay. Flow cytometry and Annexin V The apoptosis rate and cell cycle of each cell were detected by FITC / PI double staining. The expression of Bcl-2 and Bax in each cell line was detected by Western blot. Results: 1 and Wenyujin diterpenoid C had certain inhibitory effect on gastric adenocarcinoma cells with different degrees of differentiation, showing the concentration-dependent inhibition of SGC-7901, while the inhibitory effect on human GES-1 and HUVEC The role is relatively insignificant. 2 Wen Yujin diterpenoid C on the three kinds of gastric cancer cell lines were inhibited cell cycle. 3 Wen Yujin diterpenoid C can effectively induce apoptosis of gastric adenocarcinoma cell line, its role is also a certain concentration-dependent; the most obvious effect on SGC-7901. Diclofenac can inhibit the expression of anti-apoptotic protein Bcl-2 and up-regulate the expression of pro-apoptotic protein Bax in a dose-dependent manner in a concentration-dependent manner. Conclusion: Diclofenac can inhibit the proliferation of gastric cancer cells through the cytotoxic effect and the inhibition of gastric cancer cell division cycle in a safe concentration range of GES-1 and HUVEC. By down-regulating Bcl-2 and Up-regulate the expression of pro-apoptotic protein Bax to induce apoptosis of gastric cancer cells and thus exert its anti-gastric cancer effect.