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作 者:刘俊松[1] 刘翔龙 仇广林[1] 张正良[3] 樊林[1] 赵伟[1] 贺仕才[1] 常帅[1] 车向明[1]
机构地区:[1]西安交通大学医学院第一附属医院普通外科,陕西西安710061 [2]甘肃省庆阳市人民医院肿瘤外科,甘肃庆阳745000 [3]西安交通大学医学院第二附属医院急诊科,陕西西安710004
出 处:《南方医科大学学报》2015年第9期1234-1238,共5页Journal of Southern Medical University
基 金:国家自然科学基金(81172357)~~
摘 要:目的探讨β-榄香烯对胃癌细胞增殖和凋亡的影响及其可能的分子机制。方法通过四甲基偶氮唑盐比色法(MTT)、流式细胞术检测细胞凋亡、周期分布和平板克隆形成实验检测β-榄香烯对SGC7901胃癌细胞的影响,同时评价β-榄香烯对正常胃黏膜上皮细胞GES-1的毒性作用;通过Western blots检测β-榄香烯对SGC7901胃癌细胞的蛋白表达影响。结果β-榄香烯显著抑制SGC7901胃癌细胞的活性并诱导细胞凋亡,两种作用在正常胃黏膜上皮细胞GES-1中明显减弱。β-榄香烯降低SGC7901胃癌细胞克隆形成率,诱导SGC7901细胞发生G2/M期阻滞。β-榄香烯降低了SGC7901胃癌细胞Bcl-2蛋白表达水平,增加了Bax和活化的Caspase-3(17Kd)表达水平。β-榄香烯对SGC7901胃癌细胞Pak1(p21-activated protein kinase 1)的总蛋白表达无明显影响,但降低了Pak1(Thr423)和ERK1/2(Extracellular signal-Regulated Kinase 1/2)的磷酸化水平。结论β-榄香烯抑制胃癌细胞增殖,诱导胃癌细胞凋亡,其可能的分子机制为抑制Pak1/ERK信号通路的活化、调控Bcl-2和Bax等凋亡相关蛋白表达。Objective To investigate the effects of β- elemene in suppressing the proliferation and apoptosis of SGC7901 gastric cancer cells in vitro and explore the underlying mechanisms. Methods Using MTT assay, flow cytometry, and clonogenic survival assay, we assessed the effects of β-elemene on the viability, apoptosis, cell cycle distribution, and clonogenic survival of gastric cancer SGC7901 cells and gastric mucosal epithelial GES- 1 cells. Western blotting was employed to determine the changes in the protein expression profiles in SGC7901 cells in response to β-elemene treatment. Results β-elemene significantly suppressed the cell viability and increased the apoptosis of SGC7901 cells, and these effects were less obvious in GES-1 cells. β-elemene decreased clonogenic survival of SGC7901 cells, increased the proportion of G2/M phase cells, decreased the expression of Bcl- 2, and increased the expression of Bax and cleaved caspase- 3. β- elemene did not obviously affect the expression of total p21-activated protein kinase 1(Pak1) but decreased the level of phospho-Pak1(Thr423) and phospho-ERK1/2(Thr202/Tyr204) in SGC7901 cells. Conclusion β- elemene inhibits the proliferation and induces apoptosis of gastric cancer cells possibly by inhibiting Pak1/ERK signaling and regulating apoptosis-associated proteins such as Bcl-2 and Bax.
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