摘要
目的探讨胃癌细胞中活性氧(ROS)/单磷酸腺苷激活的蛋白激酶(AMPK)/信号转导与转录活化因子3(STAT 3)信号通路在熊果酸抑制环氧化酶2(COX-2)表达中的作用。方法在人胃腺癌细胞株SGC-7901中加入不同浓度熊果酸(0、10、20、30μmol/L)培养24h,或用抗氧化剂N-乙酰-L半胱氨酸(NAC 2.5mmol/L)预处理30min后熊果酸再干预培养24h。采用荧光探针2′,7′-二氯荧光素(DCFH-DA)检测细胞内ROS水平,Western blot检测AMPK、STAT 3磷酸化水平和COX-2蛋白表达。结果熊果酸明显增加SGC-7901细胞内ROS生成和AMPK磷酸化水平,抑制STAT3磷酸化和COX-2蛋白表达(P<0.01或P<0.05);而NAC能有效逆转上述各指标的变化过程(P<0.01或P<0.05)。结论熊果酸可能通过ROS/AMPK/STAT3信号转导通路抑制胃癌细胞COX-2表达。
Objective To investigate the efftect of reactive oxygen species （ROS ）/adenosine monophosphate‐activated protein kinase （AM PK ）/signal transducer and activator of transcription 3 （STAT3 ） signaling pathway on ursolic acid‐mediated inhibition of cyclooxygenase‐2 （COX‐2 ） expression in gastric cancer cell .Methods The SGC‐7901 cells were cultured with different concentrations of ursolic acid 0 ,10 ,20 and 30 μmol/L for 24 hours ,which were pretreated with N‐acetylcysteine （NAC ） 2.5 mmol/L for 30 min or were not .The intracellular level of ROS was determined by fluorescent probe 2′,7′‐dichlorofluorescein diacetate （DCFH‐DA ） and the expressions of AMPK ,STAT3 and COX‐2 were detected by Western blot .Results Ursolic acid could significantly increase intracellular production of ROS and phosphorylation level of AM PK , but inhibit phosphorylation level of STAT3 and protein expression of COX‐2 ,which were then effectively reversed by NAC （P〈0 .01 or P〈0 .05） .Conclusion Ursolic acid inhibits COX‐2 expression in gastric cancer cells probably via ROS/AMPK/STAT3 signaling pathway .
出处
《江苏医药》
CAS
2015年第12期1368-1370,F0003,共4页
Jiangsu Medical Journal
基金
国家自然科学基金(81372659)
