白术抑制胃癌细胞SGC-7901增殖并促进其凋亡

Atractylode inhibits proliferation and promotes apoptosis in gastric cancer cell line SGC-7901

目的观察白术对胃癌SGC-7901侧群细胞及非侧群细胞增殖及凋亡的影响。方法流式细胞仪分选SGC-7901中的侧群细胞;制备含白术药物血清;CCK-8法检测白术药物血清对细胞增殖能力的影响;流式细胞仪检测含白术药物血清对细胞凋亡的影响;Western blot检测药物血清对细胞中Bax及Bcl-2蛋白表达的影响;异种移植BALB/C小鼠成瘤实验观察白术对细胞体内成瘤能力影响;免疫组织化学检测白术对小鼠肿瘤组织中Bax及Bcl-2蛋白表达的影响。结果离体实验表明,含白术药物血清培养可明显降低SGC-7901侧群细胞的增殖率,同时可诱导其凋亡、分别上调和下调细胞中Bax和Bcl-2水平;在体实验显示,白术汤剂灌胃可显著抑制SGC-7901侧群细胞小鼠成瘤能力,分别上调和下调肿瘤组织中Bax和Bcl-2水平。非侧群细胞也有上述表现。结论白术可通过上调促凋亡蛋白Bax及下调抑凋亡蛋白Bcl-2从而促进胃癌SGC-7901侧群细胞及非侧群细胞凋亡,并抑制其增殖及体内成瘤能力。

Objective Investigate the roles that atractylode plays in the proliferation and apoptosis of gastric cancer cell line SGC-7901 in both side and non-side populations. Methods SGC-7901 side and non-side population cells were sorted out by flow cytometry. Following drug treatment, the effects of atractylodes on SGC-7901 cell proliferation and apoptosis were evaluated using CCK-8 assay and Annexin V/propidium iodide staining respectively. Bax and Bcl-2 expressions were further measured using Western blot. To determine the role of atractylodes in tumorigenesis, xenograft tumor formation experiment was carried out in BALB/C mice. Bax and Bcl-2 expressions in tumor tissues were detected by immunohistochemistry. Results In vitro experiments showed that atractylodes could significantly reduce proliferation, induce apoptosis, up-regulated Bax and down-regulated Bcl-2 expression in SGC-7901 side population cells. In vivo experiments showed that atractylodes could significantly inhibit tumorigenic ability of SGC-7901 side population cells in BALB/C mice, up-regulated Bax and down-regulated Bcl-2 expression in tumor tissues. The observations held true in non-side population cells. Conclusion Atractylodes can inhibit SGC-7901 cell proliferation and induce apoptosis likely through up-regulating pro-apoptotic Bax and down-regulating anti-apoptotic bcl-2. It also had an inhibitor effect on tumor formation in vivo.