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作 者:孙素霞[1] 李文军[2] 陈思强[3] 罗海吉[1] 邹飞[2]
机构地区:[1]南方医科大学公共卫生与热带医学学院营养与食品卫生学系,广州510515 [2]南方医科大学公共卫生与热带医学学院职业卫生与职业医学系,广州510515 [3]佛山出入境检验检疫局,佛山528000
出 处:《营养学报》2013年第1期27-30,34,共5页Acta Nutrimenta Sinica
基 金:国家自然科学基金(No.81202204);广东省自然科学基金(No.S2012010009467)
摘 要:目的研究丁酸钠(sodium butyrate,NaB)诱导大肠癌细胞HT-29凋亡的机制。方法 Hoechst 33342染色、Annexin V+PI和免疫印迹法检测NaB诱导大肠癌HT-29细胞的凋亡作用;激光共聚焦显微镜检测内质网(endoplasmic reticulum,ER)和细胞质中游离Ca2+浓度。结果 NaB可诱导大肠癌HT-29细胞凋亡,且具有剂量和时间反应关系;NaB浓度为2.5mmol/L,作用24h时凋亡标志分子(poly ADP-ribose polymerase,PARP)出现明显的切割片段;NaB可降低ER中游离Ca2+浓度以及升高细胞质内游离Ca2+浓度。结论 NaB可通过调节ER和细胞质中Ca2+浓度而诱导大肠癌HT-29细胞凋亡。Objective To investigate the mechanism of sodium butyrate (NAB) on apoptosis in human colorectal cancer cell line HT-29. Method The apoptosis of HT-29 induced by NaB was confirmed by hoechst33342 staining and AnnexinV+ PI assay. The concentration of intracellular and endoplasmic reticulum (ER) Ca^2+ was detected by an inverted laser scanning confocal microscope. Results NaB induced the apoptosis of HT-29 cells in time- and dose-dependence. The pro-apoptotic effect of NaB was further corroborated with the measurement of cleavage of poly ADP-ribose polymerase (PARP), A marked increase in the cleavage of PARP was noted after treatment with 2.5 mmol/L NaB for 24 h and Ca^2+ was released from ER, which in turn caused extracellular Ca^2+ influx in HT-29 cells. Conclusion The apoptosis induced by NaB in human colorectal cancer cells is correlated with the concentration of intracellular and ER Ca^2+.
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